Deliberate training with reduced carbohydrate (CHO) availability to enhance resistance training-induced skeletal muscle metabolic adaptations (i.e., the "train low, race high" paradigm) is a hot topic in sports nutrition. ( You can find a Sleep Low, Train Low nutritional periodization system in the guides .)
Low training studies involve periodic training (e.g., 30–50% of training sessions) with reduced CHO availability, where low training models include twice-daily training, fasted training, post-exercise CHO restriction, and “sleep low, train low.”
Cell signaling, gene expression, and training-induced increases in oxidative enzyme activity/protein content associated with “low training” are especially evident when training sessions begin within a specific range of muscle glycogen concentrations.
Current evidence suggests that if we want to optimize and increase gene expression to enhance fat oxidation, manipulating nutrition in conjunction with exercise is sufficient. This is necessary with the so-called "glycogen threshold," which doesn't need to be at a minimum, since these signaling pathways are suppressed when protein synthesis stops. Therefore, simply having low glycogen availability (between 100 and 300 mmol) or, in other words, using strategies like sleep-low and train-low can activate these pathways at the molecular level and enhance fat oxidation.
And what's responsible for this happening? The master regulator "PGC-1 ALPHA"
The glycogen threshold hypothesis
Adaptations associated with CHO restriction are particularly evident when pre-exercise absolute muscle glycogen concentrations are ≤300 mmol/kg dw. However, restoring post-exercise glycogen levels to >500 mmol/kg dw attenuates exercise-induced changes in gene expression (1) , and maintaining glycogen (and energy) at critically low post-exercise levels (i.e., <100 mmol/kg dw) can down-regulate protein synthesis pathways (2).
CHO feeding during exercise also attenuates AMPK-mediated signaling, but only when glycogen sparing occurs. (3 , 4)
However, it should be noted that starting exercise with < 200 mmol/kg dw is likely to impair training intensity due to the lack of muscle substrate and the impact on muscle cell contractile capacity through altered calcium regulation (5 , 6 , 7) As we have already mentioned more than once, calcium is involved in the process of contracting and relaxing the muscle (there is more information in our guide Much to talk about glycogen ).
Furthermore, repetitive daily training in the face of reduced CHO availability (to reduce muscle glycogen concentration before exercise) may increase susceptibility to disease and attenuates these pathways as discussed earlier (ketogenic diet and metabolic flexibility guide) (8).
Furthermore, repetitive daily training in the face of reduced CHO availability (to reduce muscle glycogen concentration before exercise) may increase susceptibility to disease.
In this way, the glycogen threshold provides a metabolic window of muscle glycogen concentrations (e.g., 300–100 mmol/kg dw) that is permissive to facilitate the required training intensity, acute cellular signaling responses, and post-exercise remodeling processes for metabolic flexibility.
In summary:
And how do we put it into practice?
Knowledge about this line of research is, for now, limited and highly theoretical. It can be said that there is a great gap between theory (hypothesis) and its use in practice.
With this in mind, we propose an application model for those Low-Carb workouts. But first, there's one thing to keep in mind:
- Such a severe restriction of carbohydrates and, therefore, depletion of glycogen (glycogen levels in the muscle) is not necessary to obtain the adaptations associated with this type of training.
This means that on days when we plan a Low Carb workout, an intake of around 0.8-1.2 g HC/kg of body weight in the previous servings may be adequate, without needing to restrict it to almost 0 g HC/kg as has been done before.
In this way, we will achieve the same adaptations without compromising performance and health, and without generating undesirable physiological situations (excessive catabolism, excessive metabolic stress, or problems in the immune system).
Therefore, it seems that optimizing fat oxidation does not have to be done with minimum glycogen levels (more is not always better), but with a fair amount of HC and, therefore, glycogen, the same metabolic adaptations seem to be obtained without the side effects associated with a ketogenic diet and its "adaptations" in terms of performance.
We propose an example of a diet for an athlete in the basic mesocycle 1, the goal of which is to enhance metabolic flexibility and be more efficient in specific mesocycles and competitions.
The model is presented for an elite endurance athlete (e.g., a road cyclist) who trains once daily for four consecutive days, with each session starting at 10:00 a.m. each day. In this example, the athlete has four main feeding points, and the CHO content at each time point is color-coded according to a red, amber, or green rating, representing low, medium, and high CHO intake.
Please note that we have not prescribed specific amounts of CHO and deliberately chose a RAG rating to highlight the need for flexibility in relation to the athlete's history, training status and specific training goals, etc.
In this example, a high CHO intake is recommended before, during, and after the training session on Day 1 (i.e., 'train high'), but reduced at dinner to facilitate low sleep and train low for a lower intensity session on Day 2 (i.e., you probably started with reduced muscle glycogen and withheld or reduced the CHO content of your pre-training meal).
Following completion of the second training session, high CHO availability is prescribed for the remainder of day 2 to promote glycogen storage in preparation for a higher absolute workload and intensity on day 3.
Since day 4 is a designated recovery day of much lower duration and intensity, CHO intake is then reduced on the evening of day 3 and breakfast on day 4, but then increased for the remainder of day 4 to prepare for another 4-day training block.
Careful meal-by-meal periodization (as opposed to chronic periods of CHO restriction) is likely to maintain metabolic flexibility and still allow for high-intensity, long-duration workloads during intense training.
To conclude, we must keep in mind that fats play a particularly important role. However, we often underestimate their use. We must differentiate between the types of fats we use for each occasion. For example, at dinner we can use monounsaturated (energy-producing) and polyunsaturated (structural) fats, both to recover from the previous workout and to provide energy for the next one. At breakfast before training, however, we will limit our intake of energy-producing fats and opt for structural fats.
Monounsaturated fats (energy)
Nuts, avocado or olive oil,…
Polyunsaturated fats (structural)
Tofu, edamame, soy, flax,…
Example of high food
2.5-3g/kg cho // 0.4g/kg protein // More monounsaturated and polyunsaturated fat at dinner
Breakfast 2g/kg cho //0.3g/kg protein// monounsaturated fats and salt in food
Average food example
1.5-2.5g/kg cho // 0.4g/kg protein // Poly and monounsaturated fat in dinner in equal parts
Breakfast 1-1.5g/kg cho //0.3g/kg protein// monounsaturated and some polyunsaturated fats and salt in the food
Example of food under
1-1.2g/kg cho // 0.4g/kg protein // More poly and monounsaturated fat at dinner
Breakfast 0.8-1g/kg cho //0.3g/kg protein// monounsaturated fats and salt in food
Literature
- Henriette Pilegaard, Takuya Osada, Lisbeth T. Andersen, Jørn W. Helge, Bengt Saltin, P. Darrell, Neufer. Substrate availability and transcriptional regulation of metabolic genes in human skeletal muscle during recovery from exercise DOI:https://doi.org/10.1016/j.metabol.2005.03.008
- Impey SG, Hammond KM, Shepherd SO, Sharples AP, Stewart C, Limb M, Smith K, Philp A, Jeromson S, Hamilton DL, Close GL, Morton JP. Fuel for the Work Required: A Practical Approach to Merging Low Training Paradigms for Endurance Athletes. Physiol Rep 2016;4:e12803.
- Akerstrom TCA, Birk JB, Klein DK, Erikstrup C, Plomgaard P, Pedersen BK, Wojtaszewski J. Oral glucose ingestion attenuates exercise-induced activation of 5′-AMP-activated protein kinase in human skeletal muscle. Biochem Biophys Res Commun. 2006;342:949–55.
- Lee-Young RS, Palmer MJ, Linden KC, LePlastrier K, Canny BJ, Hargreaves M, Wadley GD, Kemp BE, McConell GK. Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans. Am J Physiol Endocrinol Metab. 2006;291:566–73
- Ørtenblad N, Nielsen J, Saltin B, Holmberg HC. Role of glycogen availability in sarcoplasmic reticulum Ca2+ kinetics in human skeletal muscle. J Physiol. 2011;589:711–25
- Duhamel TA, Perco JG, Green HJ. Manipulation of dietary carbohydrates after prolonged effort modifies muscle sarcoplasmic reticulum responses in exercising men. Am J Physiol Regul Integr Comp Physiol. 2006;291:1100–10
- Gejl KD, Hvid LG, Frandsen U, Jensen K, Sahlin K, Ørtenblad N. Muscle glycogen content modifies SR Ca2+ release rate in elite endurance athletes. Med Sci Sports Exerc. 2014;46:496–505
- Costa RJ, Jones GE, Lamb KL, Coleman R, Williams JH. The effects of a high carbohydrate diet on cortisol and salivary immunoglobulin A (s-IgA) during a period of increased exercise workload among Olympic and Ironman triathletes. Int J Sports Med 2005;26:880–6.
