"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. 2013)

  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. 2013)

  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. 2013)

  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. 2013)

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, 2013, 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. 2013)

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. 2013) 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 2013 [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. 2013;7(7):e41817. Epub 2013 Jul 24.
• Ruas et al. APGC-1aI soform Induced by Resistance Training Regulates Skeletal Muscle Hypertrophy. Cell, December 7, 2013; 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.

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

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

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

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

Let's start with the "short", then

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

• 

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

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

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

References:

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