|Image 1: The "anabolic window" turns out to be more of a barn door, which is unlocked by the key of exercise and nutrition science (Random House Books)|
How to train if someone "just wants to look good naked"?
While the observations of the Coffey study (Coffey. 2005) did underline the importance of versatility, or, I should say constant "novelty", or at least modification of the training stimuli, they did not really provide any clues on how someone, who "just wants to look good naked" (and I assume this applies to the majority of non-athletes, today) should train to transform his formerly at best non-obese physique to the cover-model'ish look everybody is aspiring these days.
|Figure 1: Study design of the Vissing study with its 10-week preconditioning phase for the strength and endurance training groups (generated based on information from Vissing. 2011)|
[...] mTORC1 signaling would be selectively activated by SE [strength training], whereas AMPK signaling would be activated by both types of exercise but to a relatively higher degree after EE [endurance exercise] compared with SE [...]Thus, their research hypothesis was in accordance with the publicly accepted idea that only strength training builds muscle (obviously the role of mTOR-activation in this process is widely unknown in the general public), while endurance exercise would be the better form to train if one wanted to lose fat - as a diligent reader of the SuppVersity, you will obviously be aware that the reduction in adipose tissue you will hopefully observe, when you are dieting, is primarily a result of the depletion of muscular (and hepatic) ATP stores, which brings the AMPK energy emergency police on the scene which will concomitantly tell your muscles to suck up all extra (i.e. more than your brain needs) glycogen from your blood stream and kick your adipocytes' asses, so that they release some of their fatty energy reserves as metabolic firewood for your mitochondria.
I hope you remember "The 'hungry' side of neuronal AMPK activation", i.e. the differential effects of AMPK phosphorylation in reaction to energy shortage in muscle or liver tissue vs. its effects in the brain. If not, I suggest you (re-)read the respective passage in "AMPK III/III: Natural Rythmicity for Maximum Fat & Minimal Muscle Loss", as a thorough understanding of this difference if of utmost importance if you want to be able to compare and interpret the data from various studies correctly.The Coffey study (discussed in the last installment) did however show that this assumption, i.e. both endurance, as well as strength training will always increase AMPK, does not hold true, when we are talking about highly trained athletes - neither in the cyclists nor in the powerlifters from the Coffey study did engaging in their respective discipline produce statistically significant increases in AMPK phosphorylation.
|Figure 2: AMPK phosphorylation (0, 2.5, 5 and 22h post) and approximate area under the respective curces (small graph) during post-exercise recovery from single-bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training (data calculated based on Vissing. 2011)|
Without the AMPK elevation of an intermittent fast (or calorie reduction), it is thus unlikely that strength training alone is going to trigger significant AMPK responses.
Interestingly, the scientists state that the protein expression "of any of the reported signaling proteins" was "not altered" by the 10 weeks of pre-training, which would indicate that, contrary to years of competitive endurance exercise (cf. cyclists in illustration 1 in previous installment), 10 weeks with three weekly sessions of combined steady-state and interval exercises on stationary bikes do not blunt AMPK phosphorylation in response to 120 min of bicycle exercise at 60% of the individual VO2 max.
The induction of mTOR phosphorylation is and will remain the real strength of strength training
Likewise, the protein synthetic response (as evidenced by mTOR and p70S6K expression) did not change in response to a 10-week pre-conditioning phase comprising 30 leg workouts (3 exercises; 3-5 sets; 10 reps in the first 15 sessions, 4-6 reps in the last 15 sessions). Interestingly, and contrary to the often heard assertion that mTOR phosphorylation would be a strength training exclusive, figure 3 shows that there is still a minor, yet over the course of the post-exercise period, non-negligible increase in mTOR phosphorylation in the endurance trained subjects, whose 45min cycling session effectively blunted the mTOR dephosphorylisation the control group, who, just like all of the previously (before the preconditioning) 22 untrained healthy male subjects (79.1 kg; 182 cm; 23.3 years), fasted for the first 5h "post exercise" (their exercise consisted of sitting on the couch, doing nothing ;-).
|Figure 3: mTOR phosphorylation (0, 2.5, 5 and 22h post) and approximate area under the respective curces (small graph) during post-exercise recovery from single-bout exercise, conducted with an exercise mode to which the exercise subjects were accustomed through 10 weeks of prior training (data calculated based on Vissing. 2011)|
Strength training = opening the "anabolic barn door"
Yet, while we do now know how to unlock the barn door, we still do not know if there ain't a way to push it open even further / faster, and how to keep it wide open for as long as possible. In this context, a study by Burd et al. from Steward Phillips group at the Department of Kinesiology of McMaster University in Hamilton, Ontario (Burd. 2011) could provide further clues into the "optimal" way(s) to push the "anabolic barn door" open, as wide as possible.
After all that has been said about the over-expression of mTOR in our current society in the previous installments, it should be said that the problem does not lie with mTOR itself, as it is not the latter which inhibits AMPK, but the energy abundance that triggers the mTOR response in our western obesity scenario. This chronic nutritionally induced suppression of AMPK is something we need to distinguish from both the training-induced increase in mTOR phosphorylation and the temporary and strategically used dietary stimuli that are so characteristic of intermittent fasting.
|Figure 4: If we disregard the nutritional component, the training induced "anabolic barn door" does not only coincide with the feeding window, it would also keep you nicely "anabolic" in the course of the fasting period.|
Will the "anabolic barn door" stay open in the course of the fast and thusly prevent muscle breakdown?
This is where the data from the Burd study comes into play (Burd. 2011). In their study, Bird et al. had measured the fractional protein synthesis rate in response to feeding (15g of whey protein) and feeding and exercise (unilateral leg raises) at different intensities, i.e. 90% 1RM to failure, 30% 1RM with matched work-load and 30% 1RM to failure. What they found was that
regardless of condition, rates of mixed muscle protein and sarcoplasmic protein synthesis were similarly stimulated at FED and EX-FED (Burd. 2011)- an observation, the scientist attribute to the fact that the sarcoplasmic constituents of the muscle may be more susceptible to hydration flux, so that the results may not adequately represent the "actual" protein synthetic response.Thusly, the researchers rely in their interpretation of the data mainly on the myofibrillar protein synthesis rate (cf. figure 5).
|Figure 5: Changes (% per hour) in absolute myofibrillar protein synthesis (adapted from Burd. 2011)|
[...] protein ingestion stimulated rates of myofibrillar protein synthesis above fasting rates by 0.016 ± 0.002%/h and the response was enhanced 24 h after resistance exercise, but only in the 90FAIL and 30FAIL conditions, by 0.038 ± 0.012 and 0.041 ± 0.010, respectively. Phosphorylation of protein kinase B on Ser473 was greater than FED at EX-FED only in 90FAIL, whereas phosphorylation of mammalian target of rapamycin on Ser2448 was significantly increased at EX-FED above FED only in the 30FAIL condition.(Burd. 2011)Moreover, and this may be of even greater importance in the context of exercising on an intermittent fast, muscle protein synthesis stayed elevated way beyond what is usually considered the <4h "anabolic window".
Our results suggest that resistance exercise performed until failure confers a sensitizing effect on human skeletal muscle for at least 24 h that is specific to the myofibrillar protein fraction. (Burd. 2011)While this is obviously important for everyone who wants to accrue as much muscle muss as possible, any elevations in protein synthesis will also help a dieter to keep is hardly earned muscle, because in essence our muscles are continuously build up and broken down - proteolysis, i.e. the breakdown of muscle tissue, and protein synthesis are going hand in hand and it is the ratio of one to the other, which decides whether we are in an "anabolic" (synthesis > breakdown) or catabolic (breakdown > synthesis) state. Consequently, any elevation in protein synthesis will ameliorate muscle loss - no matter how proteolytic a dieter may become during the fasting phase.
It takes >24h for the barn door to close itself - use this time to get rid of fat, not muscle
Fine, we unlocked the "anabolic barn door", it stays open for "at least 24h"... blah blah... wtf! how does all that translate from the metaphorical into the real world of intermittent fasting? Well, the answer is pretty simple, as hundreds of trainees have been practicing exactly that with extreme success over the past couple of months:
- fast until min. 1h before your training
- spike your protein synthesis with a protein shake (~20g of whey), EAAs (~10g) or BCAAs (~8g)
- train semi-fasted and heavy
- feast within a 5-8h window
- repeat the same litany again
|Image 2: Your "anabolic barn" is huge enough to accommodate one or two steady state, low intensity or high intensity "cardio" sessions per week.|