"Mini-Fast With Exercise" a la Intermittent Fasting Can Help Minimize the "Damage" During the Holiday Season

I wonder if it is coincidence that the modern Santa is an obese advertisement character invented by some marketing genius working for Coca Cola?

Those of you who have been reading the intermittent thoughts on intermittent fasting (click here and start with the links at the bottom, if you haven't) will remember that the actual number of studies on intermittent fasting, as it is interpreted by most people on the Internet is actually quite scarce. Aside from the Ramadan studies, you mostly see very long fasting periods or other oddities that decrease the significance of the studies. That said, I did hit onto an older study that has been published in Medical Hypothesis in 2009, already. A study with a daily 12-14h "mini-fast" + low intensity aerobic exercise 5x a week and a study the results of which point to the usefulness and practical value of skipping a meal - especially in a time where you give in to nutritional temptations way too easily, anyhow - the holiday season!

Fast, walk, eat and stay lean during the holiday season and afterwards

Especially for those of you who are having some weight issues anyway, the profound body fat loss, the subjects in the Bahadori study which was based on a 7 step program comprising

* Better than monitoring total fat and GI would be to monitor your N-6 intake, emphasize mono-saturated fatty acids and eyeball the total glycemic load (the latter means potatoes are ok, but cookies are a "better stick to one" item ;-)
• a mini-fast with exercise (12–14 h) fast during every 24 h + prolonged, moderate-intensity aerobic exercise (e.g. 40-45 minutes of brisk walking) Meals are not
• no caloric restrictions, but a focus on low fat, low GI meals*
• an increased consumption in calorie-free beverages during the fast

I know that sounds stupid and 100% mainstream, but if you take a look at the data in figure 1 you will notice that it worked like a charm... well, at least for the 10 overweight men and 17 women who followed this protocol for 12 months.

Figure 1: Body weight and composition, waist and insulin levels from the beginning to the end of the 12 week non-calorically restricted 10-14 hour fast with light aerobic exercise; the asterisk (*) behind body fat (%) and insulin signifies that these values are plotted on the 2nd-ary axes (Bahadori. 2009).

Personally, I believe that one, if not the reason that this protocol worked so well were it's feasibility and flexibility, as well as being allowed to eat to satiety, when the subjects were not fasting. The 27 subjects who participated in the study were also free to chose whether they wanted to skip breakfast or dinner and switch from one to the other strategy on a daily basis to adapt their diet to their working hours and other obligations:

Coffee and teas like green, black oolong and pu-erh are your friends not just during the mini-fasts (read more).

"If participants choose to exercise in the morning, they skip breakfast and do not eat until noon. If they choose to exercise at noon, they skip lunch. If they choose to exercise in the evening, they eat an early light dinner, and then wait at least two hours to exercise (so that fasting insulin levels are restored); no food is consumed between the exercise and bedtime. (A variant of this latter strategy is to eat no dinner at all; several volunteers in the study described below adopted this approach on their own initiative.) To optimize the flexibility of this regimen, participants are allowed to switch the time of their exercise session from day to day." (Bahadori. 2009)

For your personal Christmas fast this could mean you skip breakfast tomorrow (which should not be a problem with the large Christmas dinner in your tummy), go out for a long brisk walk, have a light dinner, like a mixed salad with some cheese and chicken breast, and thus prepare yourself for the next family feast on Christmas day. If you are brunching on the day after Christmas, not a problem, you just sleep out, go for light 30min jog, shower and head over to the brunch. Eat as much as you like, and either skip dinner later or breakfast the day after.

If you are not into coffee and tea, ginger ale is another fasting friendly weight loss drink (read more).

Bottom line: To keep the damage at bay this the "mini-feast + exercise" protocol is probably feasible for anyone. It's easy, it will allow you to take part in all the Christmas festivities and won't have you sit there like an orthorexic leopard who cannot change his spots .

Whether this is a strategy worth following for longer depends on where you are at and where you want to go. If you want to look like a fitness model, it's unlikely to be sufficient to reach your goal. You will, for example, have to tweak that regimen to (a) incorporate strength training or add it in later in the day, (b) think about using a couple of supplements, such as BCAAs, caffeine and green tea during the fast and (c) eyeball the quality of the foods you eat with convenience, fast and junk-food being the exceptions to the rule of eating self-prepared whole food meals.

There are however certain downsides to protocols like this, a potential increase in adipogenesis (22% vs. 12% fat gain) and decreased lean gains (50% vs. 72%), as they were observed in a rodent study by Verbaeyes et al. (see "Eating by The Clock Could Make You Fat") with unrestricted caloric intake within the 6h feeding window, would be an example and evidence that whenever you are effectively trying to gain weight you are probably better off spreading your food intake more evenly across the day. Alternatively, you can enlarge the feeding window to 10h to maximize lean gains without the negative side effects of force-feeding yourself with 2x1,500kcal meals only twice a day or grazing continuously for 6h to meet your caloric demands.

But hey, Christmas is almost there, and there is still enough time to think about dieting and bulking after the festivities. On that note, I wish all of you a happy Christmas, a nice time with your families, friends! Regardless if you fast or not ;-)

References:

• Bahadori B, McCarty MF, Barroso-Aranda J, Gustin JC, Contreras F. A "mini-fast with exercise" protocol for fat loss. Med Hypotheses. 2009 Oct;73(4):619-22.

The IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects of PGC-1 α-4: What It Does and Why Doing Cardio Before Weights Appears to Promote It's Expression

Warning: Reading this article won't make you look like Phil Heath over night.

As announced yesterday, I am about to get back to the study on PGC-1 alpha-4, the protein Carl Lanore and I talked about in the last installment of the SuppVersity Science Round-Up on Thursday. Since I am not going to simply repeat everything I already said during the show here, I suggest you download the podcast and listen to it before you read this article. Thus you would have a basic understanding of what the Ruas' study is all about and can class the additional information this article is going to provide with the stuff you've heard on Super Human Radio. If you don't have the time or are just sitting in the office, where listening to a radio show is not really an option, I would guess that those of you who have been around on the SuppVersity for some time now, should be able to connect the dots on their own.

PGC-1 alpha-4 the missing link between myostatin, IGF-1, hypertrophy and strength gains

With the combination of in-vitro and in-vivo data from rodents and humans the study Roas et al. published in the latest issue of Cell is a seam of information - literally. Actually, this is part of the reason, why I decided to restrict the following discussion to a summary of those findings that are either of general interest or can serve as a rational foundation for practically relevant conclusions, instead of simply reiterating the whole protocol.

• 

  Figure 1: Fluorescencemicroscopy analysis of myotubes expressing GFP alone or together with PGC-1 a1 or PGC-1 a4 (left) and effects on the expression of selected RNAs (Roa. 2012)

  PGC-1 alpha and its splice variants - The four known splice variants (alpha 1-4) the scientists tested for are expressed in most of the major organs of our body. Of particular interest for our discussion here are alpha-1 and alpha-4, with the former influencing 2002 and the latter controlling 519 gene function. The overlap between the two (98 genes) is actually pretty small, so that their downstream metabolic effects can be expected to be about as distinct as their underlying triggering mechanisms.
  
  While the energy sensing system appears to be responsible for the expression of PGC-1 alpha-1 (learn more about AMPK and how your body controls glucose uptake mitochondrial activity of the cells etc. depending on the local availability of energy), PGC-1 alpha 4 expression in skeletal muscle and thus the downstream effects on myostatin (inhibition) and IGF-1 (promotion) appear to be controlled by (contractile, but also metabolic) stress. Whether this is actually the case and in how far certain overlaps do exist will yet still have to be evaluated in future studies.
  
  

  

  Figure 2: Training or overtraining - good or bad inflammation; it's often difficult to hit the sweet spot (background adapted from Kramer. 2007)

  The same goes for the exact involvement of MAPK and other stress-sensors in our bodies and the dose-response relationship between the ROS and exercise induced expression of inflammatory factors such as IL-6 => NF-KappaB and their short term beneficial effects on the training induced adaptation processes (see figure 2). What can be said for sure, though, is that over-training and the downward spiral on the right side of  figure 2 is way more likely to be the underlying cause of suboptimal results, than an absence of adequate training stimuli on the left. Adequate recovery (primarily via rest + food and not by popping supplements or suppressing your well-deserved drowsiness with stims) is therefore about as, if not more important than the one additional rep you may or may not be able crank out at the end of an intense workout.

•  What exactly can PGC-1 alpha 4 do? The trends in RNA expression in figure 1 do actually give you an idea of what the ensuing effects should be, but I guess some actual data will make it even more obvious what all these gene essays mean.

  

  Figure 3: Effect of injected PGC-1 a  and DNA manipulation on muscle fiber composition and overall muscularity and phenotype of the rodents (Ruas. 2012)

  As the data in figure 3 goes to show, the effects of PGC-1 alpha 4 injections are almost identical to what you would see to a standardized hypertrophy training. And as you may remember from my dissertation on the podcast, the >17x increase in PGC-1 alpha 4 expression in response to reloading of a previously suspended hindlimb in the scientists' rodent model would confirm just that: PGC-1 alpha 4 is expressed in response to muscular overload (as it does obviously occur, when you have not moved your leg an inch for 10 days) and initiates adaptation processes that are meant to strengthen and "build" the muscle to ensure that it is up to future challenges like this.
  
  

  

  Figure 4: Immunohistochemical analysis of gastrocnemius muscle from wild-type (WT) and Myo-PGC-1 a4 animals

  Due to the fact that the effects Roas et al. observed were muscle fiber specific and quasi non-existent in muscles that are predominantly slow twitch fibers (e.g. soleus or planatris), the concomittant boost in MHCIIa and MHCIIx myosin heavy chain types you see in figure 4 may easily be misinterpreted as a "transformation" of muscle fibers. If you look closely at the immunohistochemical analysis of the gastrocnemius muscle from wild-type (WT) and Myo-PGC-1 a4 animals in figure 4 the pictures do yet speak a very different language. If anything, the amount of the very fast twitch glycolytic (only) type IIb fibers may have dimished ever so slightly. The amount of slow twitch oxidative muscle fibers, on the other hand, remained constant, while the number of both MHCIIa and MHCIIx positive myofibers increased (the same happens, as you should remember from the Intermittent Thoughts in bodybuilders and recreational trainees, as well).
   
• PGC-1 alpha 4 boosting agents include clenbuterol 5x (see Friday's "SuppVersity Science Round-Up Seconds"), forskolin 25x (both in vitro) and cold exposure (4°C) in rodent (!) brown adipose tissue.

Aside from the anti-cancer cachexia effect which is not directly related to the topic of this post, the previous paragraphs and the podcast should actually give you the most important information about this recently discovered splice variant of PGC-1 alpha, so that we can now segue into the "real-world" part of the study and take a closer look at the interactions with strength and cardio training I have been talking about on Thursday, as well.

Exercise and PGC-1 alpha 4 in real human beings

You cannot tell me that you have never heard of the notion that doing cardio not after but either before or or in-between your lifts an have its merit. If you can't remember it anyway, go back and reread "Before, After or In-Between? Study Puts Another '?' Behind the Widely Accepted 'Cardio After Weights' Paradigm."

Previous research associated PGC-1 alpha increases primarily with endurance training and, albeit to a lesser degree, glycogen depleting high intensity interval training (HIIT), or high volume resistance training. Over the years all of these training forms have been shown to contribute to mitochondrial biogenesis, a repartitioning of fiber types towards a more versatile oxidative myosin heavy chain pattern (similar to what you see in figure 4), the AMPK mediated stimulation of fatty acid oxidation and glucose uptake, angiogenesis and the prevention of muscle atrophy (Arany. 2008). The discovery of this new splice variant of the PGC-1 alpha protein does not diminish the significance of any of these results, but it does make one thing pretty obvious: Building muscle, endurance and oxidative capacity (mytochondria) are not mutually exclusive processes and it is very likely that there is a strong overlap between the metabolic and mechanic triggering processes.

It does in fact look as if the PGC-1 alpha "family" stands, if you will, at the crossroads of the aforementioned pathways with the "classic" alpha 1 variety being triggered by AMPK (and maybe other nutrient sensors) and the alpha 4 variety responding to the exercise-specific increase in stress signals. The results of the 8-week human study, Roas et al. conducted does yet show that things are - once again - not as easy as it may seem. If you look at the three training groups the subjects (the researchers don't provide details about age or training status, but probably young untrained men) were randomly assigned to...

• 

  Figure 5: Mo & Thu and Tue & Fri workouts (top) and results of the analysis of the biopsies that have been taken 48h after the last training session (Roas. 2012)

  Endurance Training (ET): During week 1, participants completed 30 min of stationary cycling at 65% VO2 peak 3 days per week. During week 2, participants completed 45 min of stationary cycling at 65% VO2 peak 3 days per week. During week 3, participants completed 45 min of stationary cycling at 65% VO2 peak 5 days per week. During weeks 4-8, participants completed 60 min of stationary cycling at 65%VO2 peak 5 days per week. 
• Resistance Training (RT): During week 1, participants were familiarized with resistance training program and practiced the movements with light weight during each of the four training sessions. During week 2, participants completed 2 sets of 8-10 repetitions to failure 4 days per week. During week 3, participants completed 3 sets of 8-10 repetitions to failure 4 days per week. During weeks 4-8, participants completed 4 sets of 8-10 repetitions to failure 4 days per week. Table S1 presents the full exercise program. 
• Combined Training (CT): The progression of the ET was the same as that described for the ET group, except that the durations were half as long as the ET group (i.e., 30min versus 60min). The progression of the RT was the same as that described for the RT group, except that the number of lifts was less the RT group. 

... as well as the exact protocol they have been following (figure 5, top), you would probably not have expected that the combined training protocol would have an edge over the higher volume resistance training in terms of both PGF-1 alpha 4 expression, as well as the decreases in myostatingthe increases in IGF-1, and the effective mean strength gains on the leg press (+30% for both with a minimal, statistically non-significant edge for the combined regimen; not shown in figure 5).

Implications: Why doing "cardio" before a workout could be beneficial

Figure 6: Free fatty acid levels before depletion (S1) and before (S2) and after (S3) exercise trial, as well as PGC1-alpha and p-AMPK expression (Psilander. 2012)

In the absence of detailed information about the increases in muscle CSA and protein content, it may be a bit too early to formulate any implications, but since the question of "doing cardio before a workout" was at the heart of an interesting discussion some of you started in the comment area to Friday's installment of the Seconds, I want to pick up on that and present a couple of garbled thoughts and references that may explain why the combined training did produce greater increases in PGC-1 alpha-4, as well as more pronounced downstream effects on myostatin and IGF-1 than the "growth specific" strength training program.

Now, one of the beauties of having your own blog with 1020 individual posts is that you can often simply refer people to previous posts such as the one from which I just copied figure 6 into this article. In fact, the title "8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists" actually gives away most of the 'secret' that's probably behind the purported benefits of a combined training regimen: Glycogen depletion!

Can I do HIIT instead? Personally I don't see any reason why you could not replace the 30min of steady state exercise with 10-15 minutes of HIIT (including active rest), but you should be aware of the fact that this will be more taxing on your central nervous system and probably more likely to result in a decrease in exercise performance on the subsequent workout, than sitting on an ergometer cycling at 60% of your VO2max. If you feel that it works for you - fine, but don't complain if in a year from now you still don't look like Mr. Olympia ;-)

Now the Psilander study does show that glycogen depletion, which is essentially what will happen (at least to a certain degree) if you perform 30 min of cardio training at a non-exhausting, but still energy consuming pace of 60% of your VO2 max before a workout does work. Without differentiating the various iso-forms of PGC-1 alpha Psilander's 5x increase in PGC-1 does yet not tell us whether we are dealing with the "right form" of PGC here. After all, the Psilander protocol involved two endurance sessions, with the first being a depletion session that was conducted on the day before the actual test and the second being a HIIT-esque exercise test (go back to the original post for more details).  Fortunately, there are 2019 other articles on the SuppVersity so that I don't even have to refer you to a study I have not already written about to add another piece to the puzzle.

A blast from the past and a glimpse into the future

On Wednesday, October 31, 2012, I wrote about the results of a study by Lundberg et al.. Again a slightly different protocol, this time with "cardio" in the morning and strength training later in the day, yet the exact same benefits in terms of PGC-1 alpha (total) expression:

Figure 7: Selected markers of mitochondrial biogenesis and protein synthesis before during and 15, respectively 180min after the resistance training bout in the AE + RE and the RE only leg (a.u.; data adapted from Lundberg. 2012)

With the more pronounced drop in myostatin in the combined training group in the Lundberg study, the only thing we would still need to further support the practical value of the more recent results from the Roas study would be a concomitant increase in IGF-1, as we would expect it, if working out in a (partly) glycogen depleted state would actually be the reason for the increase in PGC-1 alpha 4 Roas observed in the subjects of his study. Now I could copy and paste another graph, but I guess it will be enough, when I refer you back to the detailed elaborations on the connection between IGF-1 and it's muscle-specific splice variants and exercise induced beneficial, since acute and hormetic inflammation in the "IGF, MGF & Inflammation" part of the Intermittent Thoughts on Building Muscle (click here for an overview).

Please keep in mind: Regardless of the fact that previous studies did not test for the PGC-1 alpha subtypes, we cannot ignore the existing evidence that PGC-1 is not mandatory for the beneficial effects of endurance exercise on mitochondrial biogenesis (e.g. Rowe. 2012) and should therefore not overestimate the importance of PGC1 alpha 4 as the "one and only" muscle builder. I have said that before, but I guess it's important to repeat it - this is another missing link it's just like mTOR, testosterone and whatever other magic bullets people will tell you about not exclusively responsible for increases in muscle mass, mitochondrial capacity and whatever else you may just be dreaming of.

If we now add a couple of additional findings to this intellectual brew, like ...

• the 100% increase in the expression of the heat shock protein HSP72 in a glycogen depleted vs. normal leg during a workout (Febbraio. Feb 2002)
• the 150% increase of intramuscular HSP72 in response to an infusion with low doses of interleukin-6 (Febbraio. Sep 2002)
• the non-existant negative side effects of IL-6 on muscle glucose uptake in healthy individuals (Steensberg. 2003)
• IL-6's importance as a regulator of glucose metabolism during exercise (Helge. 2003; Febbraio. 2004) and it's satellite cell proliferation promoting effects (McKay. 2009) 
• the Dr. Jakyll and Mr. Hyde nature of inflammation, in general and IL-6 in particular on glucose uptake and fatty acid oxidation, when it comes to its local and temporary (=beneficial effects) vs. systemic and chronic (=detrimental effects) presence in our body (Fisman. 2010)

...we do actually arrive back at where we came from, namely the difference between training and overtraining in figure 2.

Bottom line - cardio pre-workout as an intensity technique: On the basis of these considerations you can think of doing cardio before a workout as an intensity technique that will increase the beneficial stress and thus the demand for greater adaptive responses. That the latter will go hand in hand with an increased propensity of overtraining, particularly if you are not willing to (A) supply your body with the nutrients it needs after the workout and (B) to rest for an adequate amount of time before you hit the gym again, is something of which I would appreciate if it wasn't something I had to repeat in each and every SuppVersity article, but since this is and will probably remain the #1 reason why people don't make progress physique- or performance-wise, it's still the most important take home message at least for those of you who are new to the site. I hope this did not ruin this allegedly pretty lengthy post for you and believe I am not promising too much, when I say that you are soon going to read more about this protein here - after all, it's almost certain that we are going to see follow-up studies in the months to come.

References:

• Arany, Z. PGC-1 coactivators and skeletal muscle adaptations in health and disease. Curr. Opin. Genet Dev; 2008: 426–434. 
• Febbraio MA, Steensberg A, Walsh R, Koukoulas I, van Hall G, Saltin B, Pedersen BK. Reduced glycogen availability is associated with an elevation in HSP72 in contracting human skeletal muscle. J Physiol. 2002 Feb 1;538(Pt 3):911-7.
• Febbraio MA, Steensberg A, Fischer CP, Keller C, Hiscock N, Pedersen BK. IL-6 activates HSP72 gene expression in human skeletal muscle. Biochem Biophys Res Commun. 2002 Sep 6;296(5):1264-6.
• Febbraio MA, Hiscock N, Sacchetti M, Fischer CP, Pedersen BK. Interleukin-6 is a novel factor mediating glucose homeostasis during skeletal muscle contraction. Diabetes. 2004 Jul;53(7):1643-8.
• Fisman EZ, Tenenbaum A. The ubiquitous interleukin-6: a time for reappraisal.
  Cardiovasc Diabetol. 2010 Oct 11;9:62.
• Helge JW, Stallknecht B, Pedersen BK, Galbo H, Kiens B, Richter EA. The effect of graded exercise on IL-6 release and glucose uptake in human skeletal muscle. J Physiol. 2003 Jan 1;546(Pt 1):299-305.
• Kramer HF, Goodyear LJ. Exercise, MAPK, and NF-kappaB signaling in skeletal muscle. J Appl Physiol. 2007 Jul;103(1):388-95.
• McKay BR, De Lisio M, Johnston AP, O'Reilly CE, Phillips SM, Tarnopolsky MA, Parise G. Association of interleukin-6 signalling with the muscle stem cell response following muscle-lengthening contractions in humans. PLoS One. 2009 Jun 24;4(6):e6027.
• Psilander N, Frank P,  Flockhart M, Sahlin K. Exercise with low glycogen increases PGC-1agene expression in human skeletal muscle. Eur J Appl Physiol. 02 Oct 2012 [ahead of print]
• Rowe GC, El-Khoury R, Patten IS, Rustin P, Arany Z. PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle. PLoS One. 2012;7(7):e41817. Epub 2012 Jul 24.
• Ruas et al. APGC-1aI soform Induced by Resistance Training Regulates Skeletal Muscle Hypertrophy. Cell, December 7, 2012; 151:1319–1331.
• Steensberg A, Fischer CP, Sacchetti M, Keller C, Osada T, Schjerling P, van Hall G, Febbraio MA, Pedersen BK. Acute interleukin-6 administration does not impair muscle glucose uptake or whole-body glucose disposal in healthy humans. J Physiol. 2003 Apr 15;548(Pt 2):631-8. Epub 2003 Mar 14.

New "Fasted Cardio"-Study Falsifies the Myth of Superior Long-Term (4 Week) Fat Loss on a Moderate Energy Deficit

If we go by the convincing results of the study at hand, the fasted cardio myth is obviously busted.

Sometimes the day you've been waiting for comes faster than you'd thought... no, I am not talking about a teen's eighteens birthday or Christmas (reminds me, I still have to buy a ton of presents), but rather of the recently hinted at "fasted cardio study" by Brad Jon Schoenfeld, Alan Albert Aragon, Colin D Wilborn, James W Krieger and Gul T Sonmez.

The study of which I wrote only 2 days ago in my article about the 50% increase in fatty acid oxidation in fasted vs. fed morning cardio (learn more). And it is in fact the study which may finally solve the "Is fasted cardio good for your weight loss?"-question.

In contrast to the previously discussed paper, Schoenfeld et al. who started with the common hypothesis that "performing aerobic exercise after an overnight fast accelerates the loss of body fat" (Schoenfeld. 2014), did not content themselves with measures of acute fatty acid oxidation. What they did was a study to investigate the actual changes in fat mass and fat-free mass following four weeks of volume-equated fasted versus fed aerobic exercise in young women adhering to a hypocaloric diet.

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Needless to say that this study has the potentially to give us reliable insights with respect to the previously formulated question, because their subjects, twenty healthy young female volunteers were randomly assigned to 1 of 2 experimental groups,

• a fasted training (FASTED) group that performed exercise after an overnight fast (n =10) or
• a post-prandial training (FED) group that consumed a meal prior to exercise (n =10)

not for one or two testing days, but for 4 weeks! The training itself consisted of 1 hour of steady-state aerobic exercise on a regular treadmill (0% incline) and was performed for 3 days per week for the previously mentioned total study duration of 4 weeks.

"Subjects performed a warm-up for the first 5 minutes at an intensity equating to 50% of maximal heart rate (MHR), determined by the formula 220 - age, then increased intensity to 70% MHR for the next 50 minutes, and finished with a 5 minute cool down at 50% MHR. Heart rate monitors (model F7U, Polar Electro Inc, Lake Success, NY) were used to ensure that exercise remained at the appropriate intensity." (Schoenfeld. 2014)

To ensure that (a) the subjects actually trained and they would (b) only do the prescribed standardized volume of exercise, all training sessions were supervised by research assistants who were upper level undergraduate students in exercise science and the subjects were instructed to refrain from performing any additional structured exercise for the duration of the study.

One thing to consider: I would not fully discard fasted cardio, yet. Even if the resulrs of the study are convincing. It's one study that simulates a specific scenario. In a real world scenario you will often have people, who do shorter fasted cardio sessions, extend the fast and thus reduce their overall energy intake. This is similar to breakfast skipping, which works magic if you don't compensate for the lack of energy intake in the AM (learn more). In the study at hand this "side effect" of morning cardio didn't exist, because of the standardization of the dietary intakes of the female participants. This is perfectly correct from a science perspective, but may still be a reason the real world results you or your clients see may differ from the null-result in the study at hand.

Subjects were provided with customized dietary plans designed to induce a caloric deficit. In that, their total caloric intake was calculated on the basis of the Mifflin-St. Jeor Equation, which yields adequate, but obviously not 100% precise measurements of the resting metabolic rate (max. 10% off in non-obese adults according to Frankenfield. 2005). Since the same method was used for both groups, any possible inaccuracies, due to which the real caloric deficit among the women may not be identical to the calculated one, should carry no real weight, though. And we can simply assume that all women were in the same ~500kcal/day energy deficit the researchers thought to create.

Figure 1: Nutrient composition and total energy intake of the subjects in both groups (Schoenfeld. 2014)

In addition to their regular diet, the adherence to which was monitored on a regular basis, the subjects received a meal replacement shake either

• immediately prior to exercise for the FED group or
• immediately following exercise for the FASTED group,

with this nutritional provision carried out under the supervision of a research assistant. The "Pursuit Recovery" (Dymatize Nutrition, TX) shake you could also buy at your local GNC contains 250 calories, total, and 40 g carbohydrate (from maltodextrin and organic cane sugar), 20 g protein (from whey protein isolate + added leucine), and 0.5 g fat (residues).

Let's  take a look at the results now

As you can see in Figure 2, both groups showed a significant loss of weight (P =0.0005) and fat mass (P =0.02) from baseline, but no significant between-group differences were noted in any outcome measure (which means, that all the differences you see are "random").

Figure 2: Pre- vs. Post-study body composition measures (Schoenfeld. 2014)

As Schoenfeld et al. rightly point out, their findings clearly "indicate that body composition changes associated with aerobic exercise in conjunction with a hypocaloric diet are similar regardless whether or not an individual is fasted prior to training" (Schoenfeld. 2014) - in other words, in this pretty realistic scenario (I hope nobody starves himself after a 1h morning cardio session for another 4-8h) the myth that morning cardio on an empty stomach would accelerate fat loss is thus busted.

Bottom line: The assumption that the consumption of an insulinogenic pre-workout meal as it was used in the study at hand and a subsequent reduction of fatty acid oxidation during the workout would induce a shift from fat to carbohydrate oxidation (not measured in the study at hand, but previous studies show that this is the case) and have significant effects on an individual's long-term fat loss on an energy reduced diet is thus falsified.

The study at hand shows that the 50% increase in fatty acid oxidation w/ fasted cardio does not translate into increased fat loss | more

You could still argue that it may be beneficial if there is no energy deficit involved, for example by improving glucose levels as it was reported by Van Proeyen et al. (2013) in a study with a hyper-caloric energy intake (~bulk), but that's a whole different story.

Or you could argue that there is an albeit non-significant trend for an increased loss of fat mass in the FASTED group (inter-group difference = 33%, but the latter was (a) paid dearly for by an almost 2x higher increase in lean mass loss (inter-group difference = 60%) and stands (b) in contrast to the non-significant greater reduction in abdominal fat in the FED group as it is signified by changes in waist circumference.

For the time being, the long-standing "myth" that fasted cardio would lead to a significant acceleration has thus to be considered "questionable", if you put 100% faith the statistical accuracy of the study at hand (with only 10 participants in both groups, I am inclined not to do that) even "busted". For so long, at least, until another study, maybe one with more participants (which would allow to really figure out how "significant" the difference actually was), but a similar strict standardization, will show that it works. In that case, we would have to find out could have been that made the difference - could be the sex or training status of the subjects, the extend of the caloric deficit, the total protein intake (which was comparatively low), the type of the pre-workout meal or the form of cardio training that was used... Comment on Facebook!

References:

• Frankenfield, David, Lori Roth-Yousey, and Charlene Compher. "Comparison of predictive equations for resting metabolic rate in healthy nonobese and obese adults: a systematic review." Journal of the American Dietetic Association 105.5 (2005): 775-789.
• Van Proeyen, Karen, et al. "Training in the fasted state improves glucose tolerance during fat-rich diet." The Journal of physiology 588.21 (2010): 4289-4302. 
• Schoenfeld, Brad, et al. "Body composition changes associated with fasted versus non-fasted aerobic exercise." Journal of the International Society of Sports Nutrition 11.54 (2014)

Want to Clean Up Cellular Garbage? Train Fasted! Fasted Training Boosts Cellular Housekepping (=Autophagy) & Forms the Basis of Structural Adaptations to Exercise

Want to promote muscular and overall health? Do this after an 8h+ fast.

Exercise is a stressor. It modifies the intra and extracellular millieu, impairs the energetic status and stretches, sometimes even over-stretches the membranes. That certainly sounds as if you want to avoid it at all costs, but as nature had it, it is this eustress (good stress) that is absolutely essential for the remodeling of the muscle we are all working out for to happen - no stress no reason to adapt. It's that simple and does still have one major caveat: Too much stress and the adaptation turns into a constant and often insufficient repair process.

But who wants to "deconstruct" muscle, anyway?

Now, from the gymbro perspective the most important aspect of the training induced adaptation processes would probably be protein synthesis. And while you can actually argue that this was the case if things were just about "growing", a different picture emerges, when you look at health benefits and the actual remodeling process which does necessarily begin with "demodeling", or rather the demolution of old muscle tissue - when that's happening in a controlled self-induced (by the cell) manner, scientists call this process autophagy.

Autophagy is one of the main reasons fasting is good for you

Now, when cells "kill" themselves, they usually do that for a reason. In fact, the process of autophagy must be seen as part of the general housekeeping - a part with enormous importance, as one of the possible consequences  of its failure is cancer. Moreover, it has been demonstrated only recently that autophagy is also an essential process for muscle adaptation:

Suggested read: "If a High Fat Diet was a Pill, the Lay Press Would Celebrate it as 'Exercise in a Pill'" | read more

"Autophagy is activated in skeletal muscle by numerous catabolic stimuli such as food deprivation, denervation or sepsis. However, evidence for the necessity of basal autophagy level in the maintenance of myofibrillar integrity has counterbalanced the vision of a system only implicated in muscle wasting. Very recently, the activation of the autophagy-lysosomal pathway has emerged as an essential process for skeletal muscle adaptation after endurance training (Lira. 2013)." (Jamart. 2013)

That being said, a group of researchers from the Université catholique de Louvain in Belgium set out to study whether the two major pro-apoptotic mechanisms in our lives, i.e. working out and fasting would complement each other so that their effects add up and you get the double dose of healthy - and as you have learned today "muscle (re-)building" cell death.

Can you combine it? Yes you can!

As you can see in figure 1 the answer is clear: Yes, you can - meaning you can combine fasting and exercise and achieve an even greater activation of the autophagy-lysosomal pathway .

And what about humans? Do we have reason to believe this would not happen in human beings? Of course we do, but it is actually very unlikely that there will be major differences in the intra-muscular response to fasting. Plus, we do have human studies showing related benefits that are exclusive to fasted training, already (see "bottom line").

The data in figure 1 arose from the observations the researchers made, when they had a group of rodents perform a 90 min run at a speed of 10m/min (I did not plot the increases in markers of autophagy like Gabarapl1-II, Atg12, Lc3b, Gabarapl1 and p62/Sqstm1, simply because I don't think they are useful for you - take it for granted that those were only increased in the fasted state).

Figure 1: Comparison of selected markers of celluar and mitochondrial autophagy (mitophagy) in mice before and after 90min run in the fasted or fed state (Jamart. 2013)

 For the mice half of whom had been food deprived for 8h that's actually the normal speed of locomotion and would equal a low intensity walk/jog for a human being (about 55% of VO2max). The reason the scientists picked this protocol was that it has previously been shown to be sufficient to arrive at a plateau phase when no further increases in the accumulation of autophagosome number in different skeletal muscle groups of mice submitted to exercise running can be observed (He. 2012).

---

But is this even a good thing? Now, I can already see you struggling with the idea of voluntarily inducing "catabolism" - that's stupid right? Yes, you are right, it is in fact stupid to think about autophagy this way. This is not a non-selecive process that kills valuable muscle tissue like sarcopenia, it's a necessary prerequesite for the structural integrity of your muscle (get rid of the junk, build new stuff in place) and your whole body. The ability to boost local the systemic activation of the autophagy-lysosomal pathway is thus in fact a definitive plus you don't want to miss, but don't want to overtax, either (don't do it everyday, don't do it in combination with a high caloric deficit, don't forget to refuel after the workout).

Suggested read: "3x30s High Intensity Intervals Increase mTOR & Ramp Up Marker of Protein Synthesis - Even in a Fasted State!" | read more

In 2011 van Proeyen et al. observed that training fasted does not only increase the intramuscular fatty acid oxidation in 20 healthy young volunteers, it did also and this may come as a surprise, prevent "the development exercise-induced drop in blood glucose concentration" (Van Proeyen. 2011) - the same drop in blood sugar that will make you feel exhausted and is a potential risk factor for an acceleration of the metabolic downregulation that occurs, whenever you are dieting. One year before van Proeyen et al. had already established that in times of high fat overfeeding (+30%kcal; 50% fat) only fasted training was able to increase the AMPK levels (=anti-cancer, anti-diabetic, anti-obesity effect) in young men (van Proyen. 2011).

Said study by van Proyen was by the way the first to prove that fasted training is more potent than fed training to facilitate adaptations in muscle and to improve whole-body glucose tolerance and insulin sensitivity during hyper-caloric fat-rich diet. So, I suggest you remember it, when you wake up tomorrow and think about whether you should go for a run now or rather after filling up your belly with some delicious eggs or whatever it is that you have for breakfast.

References:

• He C, Bassik MC, Moresi V, Sun K, Wei Y, Zou Z, An Z, Loh J, Fisher J, Sun Q,
  Korsmeyer S, Packer M, May HI, Hill JA, Virgin HW, Gilpin C, Xiao G, Bassel-Duby
  R, Scherer PE, and Levine B. Exercise-induced BCL2-regulated autophagy is required
  for muscle glucose homeostasis. Nature481: 511-515, 2012. 
• Jamart C, Naslain D, Gilson H, Francaux M. Higher activation of autophagy in skeletal muscle of mice during endurance exercise in the fasted state. Am J Physiol Endocrinol Metab. 2013 Aug 20. [Epub ahead of print]
• Lira VA, Okutsu M, Zhang M, Greene NP, Laker RC, Breen DS, Hoehn KL, and Yan Z. Autophagy is required for exercise training-induced skeletal muscle adaptation and improvement of physical performance. FASEB J, 2013. 
• Van Proeyen K, Szlufcik K, Nielens H, Pelgrim K, Deldicque L, Hesselink M, Van Veldhoven PP, Hespel P. Training in the fasted state improves glucose tolerance during fat-rich diet. J Physiol. 2010 Nov 1;588(Pt 21):4289-302.
• Van Proeyen K, Szlufcik K, Nielens H, Ramaekers M, Hespel P. Beneficial metabolic adaptations due to endurance exercise training in the fasted state. J Appl Physiol. 2011 Jan;110(1):236-45. doi: 10.1152/japplphysiol.00907.2010. Epub 2010 Nov 4.

Well-Stocked Muscle Glycogen Stores Not Necessary For Exercise Induced Muscle Anabolic Response. Additional 5x Increment by Post(!)-Workout Whey + Cho Supplement.

Image 1: Glycogen depleted or not,
post-workout protein, preferably from a 
leucine-rich, fast digesting and nutritionally
complete source such as whey, is a must.

It is one thing that many trainees feel they perform better, train harder or have better endurance, when they (over-)"load" their muscle glycogen stores pre-workout. And as long as their need for carbohydrates is not merely imaginary, i.e. they feel sluggish and their gym performance sucks, whenever they are training on empty glycogen stores, I am quite sure that they will also make better gains. This mechanism would yet be completely different from any immediate, yet hitherto scientifically not validated, facilitative biomolecular effect of well-stocked glycogen stores on muscular hypertrophy, as it is proposed by many advocates of preworkout or even 24/7 carbohydrate (re-)feeding.

Dr. Connelly, who talked about this issue at length in the past installments of the BodyRX Show, was kind enough to remind me that back in 2007 Coffey et al. from Stuart Phillips' group at McMaster University, in Hamilton, Ontario (Canada), conducted a study that was based on an antithetical hypothesis, i.e. whether or not commencing resistance exercise with low muscle glycogen would enhance the encoding of genes implicated in muscular hypertrophy (Coffey. 2007). Yet, while there were significant differences at rest for the glycogen depleted vs. the normal leg of the subjects, both the increased GLUT4-MRNA expression, which is a sign of an increased capacity for glucose uptake, as well as the reduced expression of atrophic atrogenes (responsible for proteolysis, i.e. protein degradation) were overridden by exercise. Now, four years later Donny Camera from the University of Melbourne presented the results of a recent colloberation with the scientists from McMaster at the American College of Sports Medicine Conference in Denver, this year (Camera. 2011). The intention of this 2nd study was to elucidate the "effect of divergent glycogen content and subsequent post-exercise nutrition on anabolic signaling target p70S6 kinase during the early recovery period" after the completion of a standardized resistance training protocol.

Illustration 1: Very simplified illustration
of the role of mTOR and p90S6K
in protein synthesis.

Did you know that p70S6 kinase is a key component of the mTOR (the mammalian target of rapamycin) signaling cascade? The activation of mTOR via branched chain amino acids (leucine in particular) has been shown to increase p70S6K phosphorylation (the phosphorylation is equivalent to 'switching' it on). In a similar vein, physical exercise can activate protein synthesis via phosphorylation (activation) of p70S6K. The degree / increase / decrease of p70S6K kinase phosphorylation is thus considered a reliable indicator of the protein anabolic response to supplement and exercise protocols.

The evening before the actual experiment was conducted, the 16 resistance-trained male subjects (~23y) who participated in the study, reported to the laboratory in order to perform a single-legged cycling exercise to fatigue. In order not to upset the thusly established difference in glyocogen content between the trained (LOW) and the untrained leg (NORMAL), the subjects consumed an identical low carbohydrate meal after the workout and had to abstain from foods until the subsequent day, when they performed 5 unilateral leg press repetitions at 80% of their personal 1RM (one-repetition-max) with both their normal, as well as the glycogen depleted (LOW) leg. Muscle biopsies were taken 1h post exercise, and subjects consumed either a 0.5l post-workout shake that consisted of 20g whey + 40g maltodextrin or placebo immediately post and 2h after the exercise regimen.

Figure 1: Increase in  p70S6K phosphorylation in 16 resistance trained males after unilateral leg press exercise in normal and glycogen depleted leg relative to baseline (data adapted from Camera. 2011)

Although the muscle glycogen content increased exclusively in the nutrient (20g whey + 40g maltodextrin) group, significant increases of phosphorylation of p70S6K one of the key regulators of protein synthesis were seen in both legs of the subjects. As my plot of the restricted data I could extract from the abstract in the conference protocol (a paper obviously has not been published, yet) indicates, this increase was augmented up to 5x in the 1-4h hour post workout window in the glycogen depleted leg. While there was still a 8x increase in p70S6K phosphorylation in the glycogen-depleted leg even in the absence of post-workout nutrient repletion, post-workout nutrient (re-)feeding turned out to be necessary to illicit any increase in p70S6K phosphorylation over baseline in the normal leg.

Note that the baseline levels of the LOW and the NORMAL leg were probably different and the 8x increase could thus have lead to an absolute level of p70S6K phosphorylation that was still lower than in the NORMAL leg..

These results do not only contradict the initially raised hypothesis that well-stocked glycogen stores would be a necessary or at least facilitative prerequisite for the muscle anabolic response to exercise to take place, they also (re-)raise the question whether "training on empty" may not after all be advantageous if ...

1. the training performance is not effected by the lack of muscle glycogen and
2. the muscle anabolic response is augmented via appropriate post-workout nutrient-replenishment

Since this conjecture is yet solely based on the relative increases in phosphorylation, the scientists cite in their abstract, it is far from being a valid scientific hypothesis. We will probably have to wait for the publication of a respective paper (or ask someone who was lucky enough to attend the presentation for the absolute values; cf. "Note...", above), to get a preliminary answer on any beneficial effect exercising in a glycogen depleted state could have. In that, I would like to add that its artificial incarnation, i.e. the induction of local glycogen depletion, as it was practiced in the study at hand, has no significance with regard to the whole body (including liver) glycogen depletion some trainees experience as a result of (over-)training and no-carb (over-)dieting. In case of the latter, it does not take a rocket scientist to be able to tell that this won't have any beneficial effect on the gains people are making in the gym.

The Anabolic Effects of HIIT: 3x30s High Intensity Intervals Increase mTOR & Ramp Up Marker of Protein Synthesis by +43% in Men and +222% in Women - Even in a Fasted State!

Image 1: While the study at hand clearly shows that HIIT, even done on an empty stomach, is anabolic, not catabolic, it appears as if women respond better to sprint exercises than men. And this assumption is not based on gene-assays but dates back to the results of a 1999 study by Esbjörnsson which showed a more pronounced CSA increase in the leg muscles of female subjects.

Not all too long ago, the general accepted consensus was that anyone whose main interest is in building muscle must abstain from any strenuous cardiovascular exercise... running on a treadmill? God-forbid! You could lose muscle. Over the last two years or so, this paradigm has began to totter, though. And now, at the beginning of 2012 I would estimate that the number of (recognized) trainers and trainees who recommend doing high intensity interval training (HIIT), if not for general conditioning, then at least as a means to shed fat, initially surpasses the number of the conventionalists who maintain that "classic cardio" training in the "fat-burning zone" was the way to go. Now, if this is not your first visit here at the SuppVersity, you should be aware that the latest scientific research supports the arguments of the advocates of HIIT. And not so much to my, as to the surprise of some researchers, this holds true not only for already well-conditioned gymrats and athletes, who want to finally pass beyond the 10% body-fat barrier, but also for the obese and metabolically deranged diabetic, who is trying to get his blood sugar under control (cf. "Hitting Diabetes With A Hammer").

The advantages of HIIT reach well beyond fat loss, but...


Moreover, a 2011 study by Naito et al., the results of which I have discussed in November 2011, shortly after it was published in Acta Physiologica (cf. "HIT Your Satellite Cells to Increase Your Gains"), already hinted at the fact that the advantages of HIIT reach well beyond its fat-burning effects. Yet although the increase in both satellite cell count and incorporation into the muscle Naito et al. observed speak for themselves, there's still rumors going round that this training style could be catabolic. In that the argument usually revolves around the notion that muscle damage is a major driving force of satellite cell recruitement and that if the latter is a necessary consequence of HIIT it would counter your efforts to build muscle. Now, aside from the fact that this argument is intrinsically flawed (I mean, what to you do in the gym, when you weight train? You break down muscle tissue!), a recently published study from the famous Karolinska Institute in Stockholm, Sweden, attests to the fact that the exact opposite is the case.

... it appears as if women could derive even greater benefit from all-out sprinting than men

Image 2: The exercise stimulus in the study was a Wingate test, one of standard procedures in exercise science.

In an earlier study from 1999 Esbjörnsson and his / her colleagues had observed that the cross-sectional area of the leg muscles of women exhibited a more pronounced hypertrophy response to sprint training than those of their male peers (Esbjörnsson. 1999). With the advent of our advanced understanding of the underlying principles of skeletal muscle hypertrophy and the central, but as those of you who read the Hypertrophy 101 know, in the current discussion possibly overemphasized position of the mammalian target of rapamycin (mTOR), Esbjörnsson et al. did now set out to examine, whether a sex-specific response of mTOR and its downstream targets could explain their previous results (Esbjörnsson. 2012).

To this ends, the scientists recruited nine men and eight women who despite participating in leasure time sports were only "in good shape" and not considered to be athletes. For the experiment the subjects reported to the lab fasted and, after a brief 1min warm-up, performed the well-known Wingate-test, which consists of three consecutive 30s all-out sprints with 20min breaks between the intervals on a braked cycle ergometer (average peak power was ~645W and ~935W for women and men, respectively, on a per-lean body-mass base, the peak and mean power was yet identical)

Figure 1: Illustration of the experimental protocol used in the study.

Before the warm-up and 140min after the 3rd sprint, Esbjörnsson et al. took muscle biopsies from the quadriceps muscles of the subjects to assess the local expression of mTOR and its downstream targets.

Figure 2: Phosphorylated AKT, mTOR, p70S6K and rpS6 (a.u.) in male and female study participants before the first and 140min after the third sprint of the Wingate test (data adapted from Esbjörnsson. 2012)

If you are not well-versed in the the intricacies of the mTOR-cascade, it appears as if the data in figure 2 would disprove the scientists' research hypothesis that "mTOR signalling is more pronounced in women than in men". After all, the increase in phosphorylated mTOR (p-mTOR) and AKT (p-AKT) in response to the three 30s seconds sprints was obviously more pronounced in the male, than in the female participants (mTOR +26% and AKT +17% greater increases; a difference which did not reach statistical significance, though).

Do women just make better use of the same stimulus?

As far as the phosphorylation of p70S6K, of which the current scientific evidence suggests that is a more appropriate measure of the "real-world" protein synthetic effect of mTOR, a completely different picture emerges. While the +43% increase in the male subjects is just about statistically significant (p = 0.04), the +222% increase in p-p70S6K in the female subjects appears to confirm what Esbjörnsson et al. already  had suspected.

Figure 3: Serum leucine and growth hormone levels at rest and after the sprints (data adapted from Esbjörnsson. 2012)

The slightly greater disappearance of leucine from the skeletal muscle of the male subjects (cf. figure 3) is yet only one of three possible explanations (and one you could counter by ingesting BCAAs, for example) Esbjörnsson et al. come up with based on the results of previous studies:

Image 3: If you look at the leg muscles
of some of the female speed skaters,
it is quite obvious that the leg muscles
of women respond pretty well to short,
intense bouts of all-out sprinting.
(the image shows Claudia Pechstein)

1. Lower accumulation of lactate and ammonia and a faster recovery of ATP levels in type II fibers of women than men
    
2. Lower levels of plasma catecholamins (=stress hormones) in response to sprint exercises in women than in men
    
3. Slower disappearance of leucine and thusly more sustained elevation of protein synthesis in women than in men

Whether it is any of these, or a combination of all three factors which is responsible for the differential response to statistically (!) not significantly different activations of mTOR and p-AKT, cannot be decided based on the available data.

An alternative explanation, which would, by the way, have real-world implications for the training practice, is (and I prefer to cite this, to avoid being accused of sexism) that...

women do not exhaust themselves as much as men during each bout of exercise and thereby elicit a smaller activation of AMPK, resulting in less inhibition of mTOR.

In view of the fact that previous studies by Esbjörnsson et al. refute this hypothesis, it appears unlike that an "over-expression" of AMPK, of which I have discussed in one of the previous installments of the Intermittent Thoughts that its locally expressed alpha-2 isoform does not inhibit the exercise induced increase in protein synthesis, anyway, could explain why similar exercise stimuli (peak and mean power per fat-free mass were virtually identical for men and women) and within the statistical margin identical mTOR responses induce a more pronounced protein synthetic response in women than in men. And whether the early(-ier) rise in serum growth hormone, which is the last possible explanation the scientists mention, has anything to do with it appears questionably, as well. After all, the data in figure 3 shows quite clearly that the overall GH response was much more pronounced in the male than the female participants.

We don't know about aliens, but for earthlings HIIT is anabolic - regardless of their sex

In essence, it does not even really matter, what the underlying cause of the sex-specific response to sprint training is. As far as I am concerned, the most significant result of the study is not the gender-difference, but the simple, yet as the scientists point out "novel" finding that "repeated 30-s all-out bouts of sprint exercise, separated by 20 min of rest, increased Akt- mTOR signalling in skeletal muscle." And this effect was observed in both men and women. Now, this is allegedly not exactly your "usual" HIIT protocol, if you do yet take into consideration that it was performed after an overnight fast and went without BCAAs, protein shakes all the other "obligatory" anti-catabolics, the average gymrat uses to avoid the purported catabolic effects of high intensity conditioning work, I would dare to say that it HIITs another (if not a final) nail into the lid of the casket of the "HIIT = catabolic" myth.

Non-Fasted Cardio the True Key To Weight Loss? Study Shows Significant Increase in Total Energy Expenditure W/ Fed vs. Fasted Cardio - High Protein Adds to the Effect

Cardio & weight training are not mutually exclusive | learn more!

It's actually quite funny. A few days ago I wrote in a short blurb for the daily SuppVersity Classic Article that the "never-ending debate" about fasted cardio "has lost some of its momentum when the HIIT craze hit the fitness community" and today I get the following message from Päivi (thx!):

"This study totally contradicts my experience of fasted cardio. I've noticed that the best way for me to shred fat is to do fasted interval cardio, not fed one" (SuppVersity reader Päivi. March 24, 2014 | via Facebook).

"This study", in this case, refers to a soon-to-published paper from the University of Arkansas Päivi read about in a press release.

You can learn more about cardio at the SuppVersity

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4x4 = Optimal HIIT Timing?

Fasted Cardio & Beyond

In the corresponding experiment the researchers from the Human Performance Laboratory tested the differential effects of (A) fasted cardio, (B) cardio after the ingestion of a high (45%) protein meal, and (C) cardio after the ingestion of a low (15%) protein meal on the total energy expenditure of ten active (defined as burning between 500 kcal/wk and 2000 kcal/wk) women with normal body weight. And what they found is ... well, when you think about it, it's less amazing than it may appear.

Figure 1: Average metabolic rate (ml/kg/min) after the ingestion of high protein, low protein or no meal (fasted) and 40 min of cardio (5 min warm up, 30 min @60% VO2max, 5min cool down) in physically active young women (Binns. 2014)

If you take a closer look at the data in Figure 1 (and discard my analysis to the right), it may at first in fact look as if it was idiotic to do fasted cardio, if you could expend more energy if you had

• 120g of delicious oatmeal, 20oz 2% milk and a slice of wheat bread with 9g of reduced-fat peanut  butter (low protein meal), or
• 68g protein powder, 16oz of whole milk, 225g of Greek yogurt and 18g of reduced-fat peanut
  butter (high protein meal)

before the workout and still expend more energy. Now that's right: At first this may look idiotic, but if you take into account that these yummy breakfasts had slightly more than 800kcal it's highly questionable that the ~20% increase in total energy expenditure during the (presumably) 115min window that's illustrated in Figure 1 would compensate the additional energy intake of 800kcal; after all that's >50% of the lean ladies' daily basal energy requirements - a plus that would certainly not be compensated during the rest of the day.

If you want to lose weight forget about fasted or fed cardio and follow these 9 simple rules

Let's take a parting look at a pathetic increase in energy expenditure: If we do some additional math and sum up the ~6-7ml/kg/min "extra" energy expenditure for the whole 115min period (obviously that would be inappropriate because the difference is lower in the beginning), we find that the extra energy that may have looked like the solution to your "love handle problems" when you first read the abstract amounts to only ~120kcal (de facto we are probably dealing with max. 80kcal).

This leaves the ladies in the study at hand with an extra energy intake of 680kcal or 45% of their basal energy requirements. Needless to say that this was to increase energy expenditure during and after a workout is not necessarily conducive to your weight loss goals.

References:  

• Binns, Ashley, Michelle Gray, and Ro Di Brezzo. "Thermic effect of food, exercise, and total energy expenditure in active females." Journal of Science and Medicine in Sport (2014).