Luis Martinez Mora: Deliberate training with reduced carbohydrate (CHO) availability to enhance resistance training-induced skeletal muscle metabolic adaptations (i.e., the 'train low, compete high' paradigm) is a hot topic in sports nutrition. ( You have a Sleep Low, Train Low nutritional periodization system in the guides .)
Low training studies involve periodic training (e.g., 30 to 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 along with exercise is sufficient. This is necessary with the so-called "glycogen threshold," which doesn't need to be at its minimum since these signaling pathways are suppressed when protein synthesis stops. Therefore, simply having low glycogen availability (between 100 mmol and 300 mmol), or using strategies like low sleep/low training, is enough to activate these pathways at the molecular level and enhance fat oxidation.
And who is responsible for this happening? The master regulator "PGC-1 ALFA"
The glycogen threshold hypothesis
The adaptations associated with carbohydrate 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) may reduce the regulation of protein synthesis pathways (2).
Carbohydrate intake 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 a lack of muscle substrate and the impact on the contractile capacity of muscle cells through altered calcium regulation (5 , 6 , 7) Calcium, as we have already mentioned more than once, is involved in the process of muscle contraction and relaxation (you have more information in our guide, Much to Talk About Glycogen ).
Furthermore, repetitive daily training in the face of a reduction in the availability of CHO (to reduce muscle glycogen concentration before exercise) can increase susceptibility to disease and attenuates these pathways as we discussed earlier (ketogenic diet guide and metabolic flexibility) (8).
In addition, repetitive daily training in the face of reduced CHO availability (to reduce muscle glycogen concentration before exercise) may increase susceptibility to the 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 cell 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 currently limited and highly theoretical. It can be said that there is a significant gap between the theory (hypothesis) and its practical application.
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 (levels of the same 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 meals may be adequate, without needing to restrict it to almost 0 g HC/kg as has been done previously.
In this way, we will allow the same adaptations to be obtained without harming 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 minimal glycogen levels (more is not always better), but rather with a fair amount of carbohydrates and, therefore, glycogen, the same metabolic adaptations can be obtained without the side effects associated with a ketogenic diet and its performance "adaptations".
We propose an example of a diet for an athlete in the basic mesocycle 1 whose objective is to enhance metabolic flexibility and be more efficient for specific mesocycles and competition.
The model is presented for an elite endurance athlete (e.g., road cyclist) who trains once a day for four consecutive days, with each session starting at 10:00 AM. In this example, the athlete has four main feeding points, and the carbohydrate content of each time point is color-coded with a red, amber, or green rating, representing low, medium, and high carbohydrate intake, respectively.
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 (e.g., 'train high'), but reduced at dinner to facilitate low sleep and low training for a lower-intensity session on day 2 (i.e., probably started with reduced muscle glycogen and withholding or reducing the CHO content of the pre-workout meal).
After completing the second training session, a high availability of CHO is prescribed for the remainder of day 2 in order to promote glycogen storage in preparation for a greater workload and absolute intensity on day 3.
Since day 4 is a designated recovery day of much shorter duration and intensity, CHO intake is then reduced on the evening of day 3 and breakfast of day 4, but then increased during the remainder of day 4 to prepare for another 4-day training block.
Careful day-by-day 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 in intense training.
In conclusion, we must keep in mind that fats play a particularly important role. However, we often underestimate their importance. We need to differentiate between the types of fats to use at different times. For example, at dinner we can use monounsaturated (energy-providing) 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 should limit our intake of energy-providing fats and opt for structural fats.
Monounsaturated fats (energy)
Nuts, avocado or olive oil,…
Polyunsaturated fats (structural)
Tofu, edamame, soy, flax,…
Example of a high-calorie meal
2.5-3g/kg carbohydrates // 0.4g/kg protein // More monounsaturated fat and polyunsaturated fat at dinner
Breakfast: 2g/kg carbohydrates // 0.3g/kg protein // monounsaturated fats and salt in lunch
Example of a medium meal
1.5-2.5g/kg carbohydrates // 0.4g/kg protein // Polyunsaturated and monounsaturated fat in equal parts at dinner
Breakfast: 1-1.5g/kg carbohydrates // 0.3g/kg protein // monounsaturated and some polyunsaturated fats and salt in the meal
Example of a low-calorie meal
1-1.2g/kg carbohydrates // 0.4g/kg protein // Polyunsaturated fat (more polyunsaturated fat) at dinner
Breakfast: 0.8-1g/kg carbohydrates // 0.3g/kg protein // monounsaturated fats and salt at lunch
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.
