Low Carbohydrate Training

Training hungry.

Introduction

Fundamentally, there are 3 pillars of endurance training: long/slow distance sessions, interval sessions, and tempo sessions. Granted, there is substantial scope for variation under those 3 themes, but ultimately the training “formula” is fairly standard. Programming also tends to focus on 3 principal variables: volume, intensity, and frequency.

I don’t expect this to be news to anyone. However, in light of recent understanding, it seems apt that we amend that list. Specifically, the introduction of “adaptive” sessions2 and nutritional modulation around training seems warranted.

Lessons from Molecular Biology

The majority, if not all endurance adaptations are under the remit of a protein known as “PGC-1α”. This transcriptional coactivator functions almost like a volume dial, regulating the transcription* of whole host of DNA products22. As such, PGC-1α has been termed the “master regulator of mitochondrial biogenesis and energy expenditure”7.

*NB: Transcription is the first stage in gene expression, and involves writing a strand of RNA that can be subsequently translated into a amino acid/protein.

As such, the primary aim of endurance training, whether we are aware of it or not, is to increase the production & activity of PGC-1α2. An appreciation of this process can, amongst other things, yield considerable insight into the mechanistic basis behind many training practices. While I don’t expect the finer details of molecular biology to be of interest to readers here, the implications might be…

PGC-1α can explain:

Why long, slow distance (LSD) training works
via the enzyme CAMK19
Why high-intensity training also works
via the enzyme AMPK (and p38 MAPK)8
Why long-term calorie restriction might make you live longer (and why red wine, or rather resveratrol, might have a similar effect20)
via the enzyme SIRT116
Why training in the heat can, in and of itself, enhance performance
via both SIRT1 & AMPK17 + the effects of adrenaline4,18
Why you probably shouldn’t take high-dose multivitamins or synthetic antioxidants21
reactive oxygen species (or “free radicals”) are an important stimulus for PGC-1α transcription13

This understanding has also spawned interest in a novel training practice: training under conditions of low carbohydrate availability (otherwise known as “train-low, compete-high”9, which seems to stimulate similar signaling processes to high-intensity exercise, i.e. those associated with AMPK & p38 MAPK)10.

Low Carbohydrate Training

It is well established that endurance performance is influenced by initial carbohydrate availability3, hence the custom of ‘carb-loading’ prior to competition. Likewise, the consumption of carbohydrates during exercise can also improve performance14. However, these strategies may not be optimal in terms of cellular adaptation.

Adaptation results from the accretion of certain proteins involved in metabolism (e.g. metabolic enzymes, mitochondria, blood vessels etc.), and the transcription of these proteins seems to be augmented by low nutrient availability11. This should come as no surprise; the body adapts to stress, and reduced energy availability constitutes a sizeable stress.

There are two means of manipulating carbohydrate availability; targeting either endogenous or exogenous carbohydrates. “Endogenous” carbohydrates are those that are stored within the body (“endo” comes from the greek for “within”), i.e. muscle and liver glycogen. “Exogenous” (“exo” = “outside”) carbohydrates are those that are, in effect, blood-borne—originating from either dietary sources or the breakdown of liver glycogen.

Some Research: Low Muscle Glycogen (Endogenous)

Hansen et al. (2004)9
  • 7 untrained young men, 10 wks of leg extension training, consisting of 1 hr at a predetermined intensity.
  • Experimental conditions were applied to each leg.
  • Low glycogen leg = trained twice a day, every other day.
  • High glycogen leg = trained once a day, every day.
  • Subjects rested at the weekend.
  • Results: endurance in the low glycogen leg improved significantly more than the high glycogen leg, and carbohydrate storage + markers of carbohydrate metabolism also improved to a greater extent in the low glycogen leg.
Yeo et al. (2008)23
  • 14 trained male cyclists/triathletes.
  • Two alternating sessions = a 1 hr 40 min “aerobic” session & an interval session (8x 5 min w/ 1 min recovery).
  • 3 week intervention, 6 sessions per week (Sunday off).
  • Low glycogen group = performed both sessions on the same day, with 1–2 hrs in between, every other day.
  • High glycogen group = performed the sessions on different days, every day.
  • Results: the “quality” of the interval session was much lower in the low glycogen group* (unsurprisingly), but they were comparable in terms of their improvement in a 1 hr cycling trial. In addition, selected markers of adaptation (e.g. enzyme activities) and whole body fat oxidation rates were significantly higher in the low glycogen group.

* This difference only existed for the first 2 weeks, by the third week the low glycogen group seemed to have “adapted” and were achieving similar power outputs during the interval sessions as the high glycogen group.

Hulston et al. (2010)12

Using an identical protocol, this study confirmed the findings of Yeo and colleagues (above). What this study added, however, was a more detailed description of the metabolic adaptations to low glycogen training; specifically, they observed an increase in intramuscular fat oxidation and glycogen sparing.

Exogenous Carbohydrate Manipulation

Recall that “exogenous” carbohydrates are those that are present in the blood stream (they are “outside” the muscle). Therefore, reducing exogenous carbohydrate involves either limiting carbohydrate consumption (i.e. energy drinks, gels…), or training while fasted (e.g. first thing in the morning before breakfast).

While the rationale for restricting carbohydrate intake during exercise is sound as far as adaptation is concerned, research findings have generally shown no benefit11. Similarly, there is little evidence showing a benefit to training while fasted (e.g. ref. 6).

Furthermore, regarding carbohydrate supplementation during exercise, athletes also need to consider training their gut. For endurance events lasting over ~90 min, the ability to absorb and metabolise carbohydrates is a key factor in performance14. The rate-limiting step in that process seems to be gut absorption15, and regularly consuming carbohydrates during training can enhance this5. Therefore, athletes should not neglect regularly practicing race nutrition strategies for this + a whole host of other reasons.

Applications

It seems logical that athletes should look to incorporate glycogen-depleted training into their routines. Based on present understanding, and the available evidence, this could either directly enhance performance, or at least potentiate subsequent gains.

Implementing this is quite straightforward—most athletes will have been made fully aware, thanks to the solicitous efforts of nutrition companies, that you must consume carbohydrates immediately after exercise to restore glycogen. Low glycogen training, then, requires that two successive sessions be undertaken with minimal intervening carbohydrate intake (+ no carbohydrate supplementation during activity).

For example:

  • Double days: session in the morning, followed by a session in the afternoon/evening, with restricted carbohydrate intake in between.
  • Evening-Morning: session in the evening, then a session the following morning, with (again) restricted carbohydrate in between.

Practical Considerations

  • Training under low-glycogen conditions will invariably feel harder, and will naturally detract from the quality of the session12,23. Thus, it seems prudent to advise that “depleted” sessions be scheduled to coincide with long/steady sessions2.
  • The use of caffeine and/or a carbohydrate mouth rinse can ameliorate the increased perception of effort2.
  • This training strategy is probably best implemented during the “base”/“preparatory” phase of training, when the focus is on volume rather than intensity.
  • The hormonal milieu that exists during glycogen-depleted training promotes the breakdown of muscle tissue1. While this is not nearly as severe as body-building forums might have you believe, it may be a penalty for those competing in non weight-bearing sports (e.g. cycling, swimming, rowing)—though it may equally be an advantage for runners. In any case, athletes should ensure adequate protein consumption around these “adaptive” sessions.

References

  1. Baar K, McGee S. Optimizing training adaptations by manipulating glycogen. European Journal of Sport Science 8: 97–106, 2008.
  2. Baar K. Nutrition and the Adaptation to Endurance Training. Sports Med 44: 5–12, 2014.
  3. Bergstrom J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol. Scand. 71: 140–150, 1967.
  4. Chinsomboon J, Ruas J, Gupta RK, Thom R, Shoag J, Rowe GC, Sawada N, Raghuram S, Arany Z. The transcriptional coactivator PGC-1α mediates exercise-induced angiogenesis in skeletal muscle. Proceedings of the National Academy of Sciences 106: 21401–21406, 2009.
  5. Cox GR, Clark SA, Cox AJ, Halson SL, Hargreaves M, Hawley JA, Jeacocke N, Snow RJ, Yeo WK, Burke LM. Daily training with high carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling. Journal of Applied Physiology 109: 126–134, 2010.
  6. De Bock K, Derave W, Eijnde BO, Hesselink MK, Koninckx E, Rose AJ, Schrauwen P, Bonen A, Richter EA, Hespel P. Effect of training in the fasted state on metabolic responses during exercise with carbohydrate intake. Journal of Applied Physiology 104: 1045–1055, 2008.
  7. Fernandez-Marcos PJ, Auwerx J. Regulation of PGC-1 , a nodal regulator of mitochondrial biogenesis. American Journal of Clinical Nutrition 93: 884S–890S, 2011.
  8. Gibala MJ, McGee SL, Garnham AP, Howlett KF, Snow RJ, Hargreaves M. Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1 in human skeletal muscle. Journal of Applied Physiology 106: 929–934, 2009.
  9. Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK. Skeletal muscle adaptation: training twice every second day vs. training once daily. Journal of Applied Physiology 98: 93–99, 2005.
  10. Hawley JA, Burke LM, Phillips SM, Spriet LL. Nutritional modulation of training-induced skeletal muscle adaptations. Journal of Applied Physiology 110: 834–845, 2011.
  11. Hawley JA, Burke LM. Carbohydrate availability and training adaptation: effects on cell metabolism. Exercise and Sport Sciences Reviews 38: 152–160, 2010.
  12. Hulston CJ, Venables MC, Mann CH, Martin C, Philp A, Baar K, Jeukendrup AE. Training with Low Muscle Glycogen Enhances Fat Metabolism in Well-Trained Cyclists. Medicine & Science in Sports & Exercise 42: 2046–2055, 2010.
  13. Irrcher I, Ljubicic V, Hood DA. Interactions between ROS and AMP kinase activity in the regulation of PGC-1α transcription in skeletal muscle cells. Cell Physiology 296: C116–C123, 2008.
  14. Jeukendrup A. A Step Towards Personalized Sports Nutrition: Carbohydrate Intake During Exercise. Sports Med 44: 25–33, 2014.
  15. Jeukendrup AE. Nutrition for endurance sports: Marathon, triathlon, and road cycling. Journal of Sports Sciences 29: S91–S99, 2011.
  16. Kim E-J, Um S-J. SIRT1: roles in aging and cancer. BMB Rep 41: 751–756, 2008.
  17. Liu CT, Brooks GA. Mild heat stress induces mitochondrial biogenesis in C2C12 myotubes. Journal of Applied Physiology 112: 354–361, 2012.
  18. Miura S, Kawanaka K, Kai Y, Tamura M, Goto M, Shiuchi T, Minokoshi Y, Ezaki O. An Increase in Murine Skeletal Muscle Peroxisome Proliferator-Activated Receptor-γ Coactivator-1α (PGC-1α) mRNA in Response to Exercise Is Mediated by β-Adrenergic Receptor Activation. Endocrinology 148: 3441–3448, 2007.
  19. Ojuka EO, Jones TE, Han D-H, Chen M, Holloszy JO. Raising Ca2#. in L6 myotubes mimics effects of exercise on mitochondrial biogenesis in muscle. FASEB J. 17: 675–681, 2003.
  20. Park S-J, Ahmad F, Philp A, Baar K, Williams T, Luo H, Ke H, Rehmann H, Taussig R, Brown AL, Kim MK, Beaven MA, Burgin AB, Manganiello V, Chung JH. Resveratrol Ameliorates Aging-Related Metabolic Phenotypes by Inhibiting cAMP Phosphodiesterases. Cell 148: 421–433, 2012.
  21. Powers S, Nelson WB, Larson-Meyer E. Antioxidant and Vitamin D supplements for athletes: Sense or nonsense? Journal of Sports Sciences 29: S47–S55, 2011.
  22. Yan Z. Exercise, PGC-1α, and metabolic adaptation in skeletal muscle. Appl. Physiol. Nutr. Metab. 34: 424–427, 2009.
  23. Yeo WK, Paton CD, Garnham AP, Burke LM, Carey AL, Hawley JA. Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens. Journal of Applied Physiology 105: 1462–1470, 2008.