Intermittent Thoughts On Intermittent Fasting - Exercise (1/3): Cycling, Powerlifting and Lean Gaining ;-)

Image 1: It may be more effective than your usual "eat half as much diet", but even with intermittent fasting exercise is compulsory, not facultative.
In the last installments of this series we have analyzed the natural interplay between AMPK and mTOR, have learned that chronic over-expression of either of the two can be detrimental to the way you look, feel and perform and have scratched on the surface of how intermittent fasting and the use of AMPK and/or mTOR promoting supplements can restore and amplify the natural up and down on the AMPK/mTOR seesaw and thus promote fat loss and and gains in lean body mass - not at the same time, but cyclically. In this episode it is high time to take a closer look on how exercise, the one and only true "body recompositioning agent", plays into this.

Tell me who you are and I tell you how your body will respond to exercise.

What we already know is that the exercise induced depletion of intra-cellular ATP and the corresponding increase in ADP and AMP levels will produce profound(!) increases in AMPK phosphorylation. In a recent study on the effects of a 30s Wingate test (a sprinting test on a cycle ergometer with breaking loads equivalent to 10 and 8% of body weight for men and women), for example, scientists from Gran Canaria found increases in AMPK phosphorylation vs. baseline of +495% - 98% for the ten women in the study and +278% - 33% for the 17 (cf. figure 1)
Figure 1: Relative changes in AMPK phosphorylation in response to 30s Wingate sprint test in 17 male and ten female subjects (data calculated based on Fuentes. 2011)
As you can see there is a huge (and statistically significant) gender difference in the initial AMPK(-alpha) response to sprinting, the difference at 30min and 120min post exercise on the other hand did not reach statistical significance (p<0.05). In an aerobic exercise scenario (90min at 60%VO2max), however, Roepstorff et al. PK came up with the exact opposite results (Roepstorff. 2006):
A 198% increase (P < 0.001) was observed from rest to 90 min of exercise in men, whereas in women the exercise-induced 74% increase in αAMPK Thr172 phosphorylation was only borderline-significant.
The different fiber-composition of the male and female subjects could provide an adequate explanation for this phenomenon. With a +23% higher ratio of slow twitch type I to fast twitch type II fibers, the women in the Roepstorff study were, on a pound per pound base, more effective endurance athletes than the men. Consequently, they did not run out of fuel so fast and thusly there was no need for their bodies to ramp up AMPK by the same 198% as the bodies of the men did.
Figure 2: Fat oxidation (in kcal/kg per min) calculated based on respiratory exchange ratio in male and female participants of a 90min cycling bout at 60% of their individual VO2Max (Roepstorff. 2006)
It is important to note that despite lower AMPK activiation in the female participants of the Roepstorff study, the women (due to their high ratio of type I fibers with +25% higher capillarization) had statistically significantly higher fatty acid oxidation rates (i.e. they burnt more fat) than their male counterparts (cf. figure 2)! This goes to show you that the metabolic scene, which is set by AMPK, is not the sole determinant of substrate metabolism. In the end, the capacity of the mitochondrial furnaces decides how much energy from fat you will be able to burn. For subjects with a high amount of type I fibers whose primary objective is to actively burn additional fat calories, aerobic exercise may thus well be a viable alternative for intense HIT regimens, of which Astorino et al. have recently shown that the rate of fatty acid oxidation in recreationally active men and women is identical within the statistical margins (Astorino. 2011).
Conversely, the higher type II to type I fiber ratio of men makes them better sprinters. That and their overall larger muscle mass could have allowed them to perform the 30s sprint on the cycle ergometer without having to resort to extra-muscular energy stores, which would explain why we did not see a significant increase of AMPK immediately after sprinting. Its occurrence 30 minutes after the sprinting exercise does yet go to show that even very short exercise bouts can trigger pretty profound AMPK responses, of which I would speculate that they facilitate post-exercise glycogen repletion via "energy-repartitioning".

Why cyclists should powerlift and powerlifters should cycle

Illustration 1: Differential response of cyclists and power lifters to strength and endurance training; statistically significant increases are highlighted in green, statistically significant decreases in red (data compiled from Coffey. 2005)
With regard to the differential response to different exercise modalities we also know from a 2005 study by Coffey et al. (Coffey. 2005) that muscle from strength-  and endurance-trained individuals respond very differently to endurance (1 h cycling at 70% VO2peak) or resistance training (8 sets of 5 maximal repetitions of isokinetic leg extensions).

I've gone to all the bother of compiling the extensive data on muscle protein synthesis and related signalling proteins from the study into a single chart (cf. illustration 1), where statistically highly significant increases are highlighted in green and statistically significant decreases are highlighted in red. Thusly, you should be able to see that if the goal is to increase AMPK, cyclists have to strength train, while powerlifters will have to get into the saddle of an elliptical or ergometer.

What appears paradoxical at first, is the result of adaptation processes: Only novel and unaccustomed stimuli trigger further adaptation... and "novelty" is such a profound trigger of adaptational responses that - under the assumption that p70S6K phosphorylation is a reliable measure of the protein synthetic training response - cycling causes almost comparable increases in protein synthesis as resistance training in powerlifters, a group of athletes who are not exactly known for doing large amounts of "cardio" training.

Since this is not exactly "intermittend fasted" related, I leave it up to you to interpret the rest of the data. Before I "think on", I do yet want to caution you against getting stuck in doing the same type of exercise over and over again - there is a reason that 99% percent of the figure athletes, bodybuilders, fitness models or whatever other athletes and celebrities you think have an aesthetic body, incorporate some form of aerobic training into their regimens, as well (if you read the latest posts on HIIT training, you will be familiar that "aerobic" does not always mean steady state endurance training ;-)

Training fasted? Maybe, for athletes and performance oriented amateurs.

While the previously discussed studies showed that AMPK/mTOR responses to different exercise regimes largely depend on who you are and what type of training you have conditioned your body to, it did not answer the question that appears to be preying on everyone's mind, which is "Do I do my aerobic and or resistance training in a fasted (no food at all), semi-fasted (only protein and maybe some fat), or fed state?" Or in other words: "Do I break the fast before or after training?"

Image 2: Ramadan fasting can serve as a relatively particularly well studied "model" of intermittent fasting. You can find more information about the strengths and limitations of this model, please read Part 2 and Part 3 of this series.
A brief reminder for all who of you who missed the first installments of this series and may now wonder why I am, without further explanations, referring to studies on Ramadan fasting as if it was intermittent fasting - in essence it is! This is why I have already discussed a handful of studies that investigated the effects of Ramadan fasting on Muslim athletes, in the initial installments of this series. In that context, I have also pointed out why the Ramadan "protocol" is an acceptable model of intermittent fasting and where it deviates from what we are seeing in the dietary regimens with which Adelfo and Duong get to grips with the little fat that is still left on their athletic bodies. For more information on that I would like to refer you to Part 2 and Part 3 of this series, in particular.
If you are a competitive athlete, who follows the advice of the establishment, the answer is easy - EAT, EAT, EAT! And do not even think of fasting! On the other hand, even experts openly admit that despite the fact that it is (Maughan. 2010).
often automatically assumed that intermittent fasting will lead to decrements in exercise performance. [...t]he available evidence does not entirely support this view, but there is little or no information on the effects on elite athletes competing in challenging environments.
With respect to the lack of data, we are in the fortunate position that the Olympic Games 2012 coincide with the Ramadan period from July 21 to August 20, 2012, i.e. right in the heart of the Games. Meanwhile we do yet have to resort to the little reliable data there is and of which Maughan et al. writes in another article that it "suggests that effects of Ramadan-style fasting on exercise performance are generally small." And a pretty recent study which investigated the effects of Ramadan fasting on performance and body composition of 16 young soccer players (17.4±1.2 years, 175.4±3.6 cm, 69.6±4.3 kg and 5.1±1.3 years of training experience) corroborates this assertion.

Study shows: You can improve body composition and performance if you train intermittendly fasted, but not in a fasted state 

Alpay Güvenc from the School of Physical Education and Sports at the Akdeniz University in Antalya, Turkey, assessed body composition, hydration status, dietary intake and sleep duration of his 16 male subjects, who continued their regular pre-season soccer training during the four weeks of Ramadan, on four occasions: before Ramadan, at the beginning of Ramadan, at the end of Ramadan and 2 weeks after the end of Ramadan. The training sessions were yet postponed, so that the soccer players could have a snack or meal before they took to the field - they were thus intermittendly fasting, but not training in a fasted state!
Figure 3: Relative changes in RD: running distance, RT: running time, RV: running velocity and
RV4.0: running velocity at 4.0mmol.L-1 lactate concentration due to Ramadan fasting during the pre-season preparations in 16 male soccer players (data calculated based on Güvenc. 2011)
As figure 3 goes to show, there was an initial decline in exercise performance in the first week of Ramadan (=intermittent) fasting. In the last week of Ramadan, the maximal running distance, the running time and velocity and the RV4 (running velocity at 4.0mmol.L-1 lactate concentration) had improved - only by 3%, 3%, 1% and 2% over baseline, but nevertheless statistically significantly. Now, what may be even more interesting for professional athletes is that these beneficial effects continued well into the post-Ramadan phase - how much of this has yet to be ascribed to the training regimen (remember the soccer players were in their pre-season preparation) could only be determined if half of the kids had been Christians and had served as a non-intermittendly-fasted control.
Figure 4: Changes in total body water (TBW in L), fat free mass (FFM in kg), body fat (in kg) and  the sum of skin-fold measures (in mm) due to Ramadan fasting during the pre-season preparations in 16 male soccer players (data calculated based on Güvenc. 2011)
In a similar vein, we cannot say for sure, whether there had been comparable improvements in body composition (as evidenced by the statistical significant reduction in skinfold measures, i.e. -2.2% by week 4 of Ramadan fasting; cf. figure 4), if the players had just continued their usual pre-season training without fasting intermittendly. What we can say for sure though, is that they achieved the latter without any major changes in their overall caloric intake or macronutrient composition (cf. figure 5)
And that the fasting had no negative effects on the subjects sleep duration (~8.7h) or their hydration status. So that, it would appear that during a metabolically demanding pre-season training a non-specific intermittent fast works just / at least as good as a normal diet, as long as the athletes meet their training induced caloric demands.

Training fasted? Yes, for lean gains.

Image 3: For some "lean gains" happen only in their heads (img
Now, while "exercise performance" obviously is an important variable, I assume most of you who are toying around with the idea of doing an intermittent fast, are more interested in its effect on body composition and would tolerate a dip in "exercise performance" (whatever type of exercise that may be in your case) if only those love handles finally disappeared and allowed your ever-increasing muscle mass to shine... or are you interested in the potential (largely AMPK-related) health benefits intermittent fasting has to offer in a world, where nutritional abundance is a 24/7 phaenomenon and the world "bulking" is often misinterpreted as taking advantage of the former as often as possible?

In both cases the results of a 2010 study from the Human Performance Laboratory in Leuven, Belgium (not the one in Canada!) would be relevant for you. In that study (Van Proeyen. 2010), Van Proeyen et al. had 27 healthy male volunteers consume a hypercaloric high-fat diet (∼+30% kcal/day; 50% of kcal from fat) for 6 weeks. Additionally 20 of the subjects had to participate in 4 training sessions per week (2x90min and 2x60min) consisting of cycling at 70-75% of the individual VO2Max and running at 85% of the maximal heart rate. 10 of the subjects (CHO; n=10) had yet had breakfast (~90min before training; 675 kcal, 70% carbohydrates, 15% fat, 15% protein), the rest (fasted; n= 10) reported to the lab after an overnight fast.
Figure 4: GLUT4 and AMPK expression in 10 healthy male subjects before and after 5 weeks on a hyper-caloric high-fat diet with or without (control) exercise in the fasted or fed (CHO) state  (data calculated based on Van Proeyen. 2010).
As the asterisk in figure 4 indicates, the exercise induced increase in GLUT4 (responsible for muscular glucose uptake) and AMPK expression is significant (p<0.05, i.e. chances that this is only coincidence <5%) only in the subjects which trained in a fasted state. Moreover, only the group which trained in the fasted state had neither statistically significant weight increases, nor statistically significant increases in the sum of the skinfold measurements (a relative reliable marker of body fat levels). The unexercised controls and the CHO group (training in fed state), on the other hand, gained 3kg and 1.4kg body weight (both p<0.05). Interestingly, though only the control group experienced a statistical significant increase in the sum of their skinfold measures of +15.1%! (+1.1% in fasted; +5.4% in CHO).
This study for the first time shows 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. (Van Proeyen. 2010).
Obviously, we are dealing with a very different situation, when an intermittent fast is combined with a caloric deficit - yet in view of the idea to use intermittent fasting as dietary strategy on a "lean bulk", the results of the Van Proeyen study could be of great importance. Not only in view of keeping the fat gains at bay, but also with regard to potential negative health effects of deliberate overeating and subsequently compromised insulin sensitivity.

A pros pos "lean bulk", I suggest you do come back next week if you want to know more about when and what to eat right after what type of workouts in order to maximize muscle and minimize fat gains when you train intermittendly fasted. For now, I wish all of you a sunny Sunday (here it is one) and an intense week at the gym, regardless of whether you train (intermittendly) fasted or not ;-)
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