True or False? 'If you Don't Eat Carbs After Your Workout, Sleep Fasted, Train on Empty You Build New Mitochondria'

Going to raid the fridge? No, you better don't do this the night after a workout. Myth says: Going to bed glycogen depleted will boost mitochondrial biogenesis - true of false?
In a world, where "tried and proven" is considered "mediocre, boring and ineffective" by many, self-proclaimed fitness experts have to become very creative to get the attention of a large audience. Next to several interesting and in some cases even promising training routines, the need to be creative also produces very dubitable recommendations, like "If you Don't Eat Carbs After Your Workout, This Will Turn You into a Fat Burning Machine!"

As any good myth, the "no carbs after your workout"-myth can be supported by cherry picking studies and ignoring the missing real-world implications of their results.
Do you have to worry about fasting when your're dieting!?

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Breaking the Fast & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review
In the case of the "no carbs after your workout"-myth, you could argue, for example, that it has been shown repeatedly that exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle (Psilander. 2013), but in that case, the mitochondrial building happened after the repletion of glyogen at the end of the workout. Now, a recent study confirms, that this, i.e. the in-/ and eflux of energy are both necessary part of the same mitochondrial biogenesis equation.
Figure 1: Overview of the study protocol in Lane, et al. (2015)
In said study, Stephen Cheyne Lane and colleagues found no evidence increases in mitochondrial biogenesis when they determined the effects of 'periodized nutrition', in this case being fed or fasted after an intense exercise session (HIT -  8 x 5 min work bouts at 82.5% of individual peak power output (PPO) with 1 min active recovery (100 W) between work bout) on skeletal muscle and whole-body responses to a bout of prolonged exercise the following morning. All in all, Lane et al. had seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion:
  • Trial 1 (FASTED) in which they consumed 8 g/kg body mass of CHO before undertaking an evening session of high-intensity training (HIT) and slept without eating,
  • Trial 2 (FED) in which they consumed half of the carbohydrates before (4 g/kg BM) and the rest (another 4g/kg BM) right after the workout and before they went to bed.
On the next morning the subjects completed 2 h cycling (120SS) before having breakfast. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on Day 2 (D2) pre-, post-, and 4 h after 2h cycling exercise during steady state exercise (120SS | subject cycled at ~60% of VO2peak). Why did the scientists go to this length? Why didn't they simply have their subjects do another exercise session 1-2h after the first? Here's the well-phrased answer Lane et al. have for you:
"A major aim of this study was to circumvent the previously observed impairment in maximal self-selected training intensity when athletes perform two bouts of training within several hours, the second session commenced with reduced muscle glycogen content (Hulston. 2010, Yeo. 2008). Under such conditions, power output is reduced by ~8% (Hulston. 2010, Yeo. 2008), even when caffeine is ingested in an attempt to offset this decline (Lane. 2013). By undertaking HIT in the evening and then withholding feeding overnight, athletes were able to complete HIT and still ‘train-low’ the following morning without compromising the total ‘training impulse’ to the working muscles" (Lane. 2015)
As you probably expected, the muscle glycogen levels of the subjects in the FED group were higher at all times after the HIT exercise on day 1 (P< 0.001). It is thus no wonder that the resting phosphorylation of AMPKThr172, p38MAPKThr180/Tyr182 and p-ACCSer79, as well as the fat oxidation during the 2 hours of steady state cycling on the second morning were higher in the FASTED group, as well.
Figure 2: Just to get that straight. The study does not say that you are not burning more fat fasted, but you know that this does not mean that you lose more body fat (see "AM Cardio Study" | figures from Lane. 2015)
Unfortunately, that's not the effect with long-term consequences in form of mitochondrial gains we all are looking for. As the authors rightly point out in their conclusion, is that
"[i]n contrast to COX4I1, the responses of some other genes with roles in mitochondrial biogenesis (PGC1α and TFAM) were not substantially altered by either dietary condition in response to the second exercise bout. [Furthermore the d]ifferences in results between the current and earlier (Psilander. 2014) study are hard to reconcile. PPARδ mRNA expression increased in the hours after exercise, but only to a significant extent during the FED trial.

Figure 3: Rel. Methylation of  PPARδ which suggest that low glycogen impairs mitochondrial building (Lane. 2015).
Correspondingly, greater methylation of PPARδ was observed in the FASTED trial 4 hours after the steady-state exercise, which may underlie the comparatively reduced mRNA expression (Figure 3).

Since high-, but not low-intensity exercise led to hypomethylation of the PPARδ gene and increased gene transcription (Barres. 2012), exercising in a fasted state may preclude the necessary glycolytic flux to induce these adaptive responses at the genomic level" (Lane. 2015 | my emphasis).
So, in other words. There are changes in DNA methylation on paper that look nice, but without the often-cited up and down of energy availability to the cells, there's no growth. To make it even more obvious: If you don't replete after depletion, you're not going to grow even though some of the growth signals may be triggered by depletion.
Intermittent Thoughts On Intermittent Fasting - Exercise (2/3): Opening the "Anabolic Barn Door" With the Key of Exercise and Nutrition Science!
And we could have known that all along. Why? Easy, mitochondrial biogenesis as an anabolic process may be triggered by an increased expression of proteins that increase when you fast, but fasting alone - animal studies have shown that conclusively - does not induce an increase in mitochondria in heart, brain, liver, adipose tissue, or skeletal muscle (Hancock. 2011).

While only a long-term study will ultimately settle the issue, the study at hand proves that depleting (=fasting by exercise) doesn't appear to have the ability to add mitochondria if it's not cycled with repleting (=feasting). Or put even more simply: Anabolism, whether it's in form of mitochondrial biogenenesis, glycogen storage, protein synthesis and what not, always depends on the cyclic nature of "energy out vs. energy in" I previously described as the mTOR - AMPK Seesaw in the IF series | Comment on FB!
  • Bassel-Duby, Rhonda, and Eric N. Olson. "Signaling pathways in skeletal muscle remodeling." Annu. Rev. Biochem. 75 (2006): 19-37.
  • Barres, Romain, et al. "Acute exercise remodels promoter methylation in human skeletal muscle." Cell metabolism 15.3 (2012): 405-411.
  • Evans, Ronald M., Grant D. Barish, and Yong-Xu Wang. "PPARs and the complex journey to obesity." Nature medicine 10.4 (2004): 355-361.
  • Fujita, Satoshi, et al. "Essential amino acid and carbohydrate ingestion before resistance exercise does not enhance postexercise muscle protein synthesis." Journal of Applied Physiology 106.5 (2009): 1730-1739.
  • Hancock, Chad R., et al. "Does calorie restriction induce mitochondrial biogenesis? A reevaluation." The FASEB Journal 25.2 (2011): 785-791.
  • Hulston, Carl J., et al. "Training with low muscle glycogen enhances fat metabolism in well-trained cyclists." Medicine and science in sports and exercise 42 (2010): 2046-55.
  • Lane, Stephen C., et al. "Caffeine ingestion and cycling power output in a low or normal muscle glycogen state." Medicine & Science in Sports & Exercise 45.8 (2013): 1577-1584.
  • Lane et al. "Effects of sleeping with reduced carbohydrate availability on acute training responses." Journal of Applied Physiology Published 25 June 2015 Vol. no. , DOI: 10.1152/japplphysiol.00857.2014
  • Psilander, Niklas, et al. "Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle." European journal of applied physiology 113.4 (2013): 951-963.
  • Yeo, Wee Kian, et al. "Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens." Journal of Applied Physiology 105.5 (2008): 1462-1470.
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