High CHO (not fat) is the way to GO in your post-exercise window
It is now generally accepted that consuming a dose of ~0.45-0.55 g of high-quality protein per kg of body weight within 3 hours of exercise (scaled with proximity to the pre-workout protein meal) is an effective strategy for maximising muscle protein synthesis, and therefore hypertrophic adaptations in muscle.
Less is known regarding the importance of carbohydrate and dietary fat dosing post exercise. Research among endurance athletes suggests that reduced carbohydrate availability post-exercise (i.e. feeding on dietary fat in place of carbohydrate) may augment some of the positive responses to the training itself. This occurs via modulation of the acute cell signalling pathways and downstream gene-expression responses associated with desired exercise adaptations – namely – enhanced mitochondrial biogenesis, increased intramuscular and whole-body fat metabolism, and improved exercise capacity and performance. Furthermore, a recent study demonstrated that consuming whole eggs caused greater stimulation of muscle protein synthesis than egg whites, despite matched protein content. This lead some to suggest that dietary fat has a pro-anabolic effect and thus may be an effective post-exercise feeding strategy.
Alternatively, another school of thought suggests that the avoidance of dietary fat post-exercise and targeted consumption of carbohydrate may be a superior approach. Grounded partly in golden-era bodybuilding “bro-lore”, many advise the restriction of dietary fat post-exercise – in theory – to maximise an insulin response coinciding with the “anabolic window” and to expedite nutrient uptake to muscle cells. The problem with this way of thinking is that more recent research suggests muscle cells have enhanced sensitivity to nutrients for far longer than originally thought post-exercise, leading some researchers to adapt the terminology from “anabolic window” to “anabolic barn door”. Thus, restricting dietary fat with the objective of maximising the rate of nutrient uptake post-exercise likely has minimal benefit, if any.
However, perhaps a more evidence-based rationale for higher carb/lower fat feeding post-exercise derives from research on competitive sports athletes. Previous studies demonstrate that inadequate carbohydrate intake can impair both strength and endurance performance and is associated with increased muscular fatigue. Consuming carbohydrate post-exercise also increases intramuscular glycogen storage, which is known to reduce recovery times. Furthermore, an influx of carbohydrate post-exercise could lead to an enhanced muscle protein synthesis response through the insulin-mediated activation of the Akt/mTORC1 pathway, and concomitant reductions in cortisol and muscle protein breakdown.
It is important for us to remember that the muscle responses to training i.e. the turnover of contractile proteins are largely controlled through the translational machinery and the mTORC1 and p70S6K1 signalling pathway. Thus, any strategy that enhances activation of these protein kinases is likely to translate to improved muscle protein synthesis and thus hypertrophic adaptation. A previous study examined the effects of reduced carbohydrate but high post-exercise fat consumption on the activation of these signalling kinases following an aerobic exercise protocol. Findings showed that post-exercise high-fat feeding was associated with suppression of p70S6K1 activity (despite sufficient post-exercise protein intake) at 3 hours post-exercise, which contrasted with an elevated response observed when participants consumed high carbohydrate/low fat post-exercise. This finding suggests that post-exercise high-fat feeding may impair the regulation of the skeletal muscle remodelling processes, thereby potentially causing undesirable adaptation if performed long-term. Now, some might suggest that these findings are limited in terms of practical application to weight lifters given the nature of the aerobic style exercise protocol. However, we have more data supporting suppressed anabolic activity following high-fat feeding. For instance, following direct infusion of lipid to cause elevation in circulating free fatty acids in the blood, muscle protein synthesis was attenuated in skeletal muscle after consumption of a 21g amino acid drink. Additionally, high-fat feeding impaired muscle protein synthesis in rats, associated with reduced p70S6K1 activation.
So, what do we make of this?
In the physiological context of the exercising human – while further research is still required – it seems wise to restrict dietary fat in your post-exercise feeding window if maximal muscle hypertrophy is the objective. A sensible practical application based on current evidence would be to limit dietary fat content to 10g or below, while consuming 0.45-0.55g of protein and approximately 1.5g of carbohydrate per kg of body weight in a meal within 3 hours post workout.
And remember guys – CHOs before hoes, but not before bros.
- Aragon, A. A., & Schoenfeld, B. J. (2013). Nutrient timing revisited: is there a post-exercise anabolic window? Journal of the International Society of Sports Nutrition, 10(1), 5. doi:10.1186/1550-2783-10-5.
- Hammond, K. M., Impey, S. G., Currell, K., Mitchell, N., Shepherd, S. O., Jeromson, S., . . . Morton, J. P. (2016). Postexercise High-Fat Feeding Suppresses p70S6K1 Activity in Human Skeletal Muscle. Med Sci Sports Exerc, 48(11), 2108-2117.
- van Vliet, S., Shy, E. L., Abou Sawan, S., Beals, J. W., West, D. W., Skinner, S. K., . . . Burd, N. A. (2017). Consumption of whole eggs promotes greater stimulation of postexercise muscle protein synthesis than consumption of isonitrogenous amounts of egg whites in young men. Am J Clin Nutr, 106(6), 1401-1412.
- Burke, L.M.; Hawley, J.A.; Wong, S.H.; Jeukendrup, A.E. Carbohydrates for training and competition. J. Sports Sci. 2011, 29 (Suppl. 1), S17–S27.
- Haff,G.G.;Lehmkuhl,M.J.;McCoy,L.B.;Stone,M.H.Carbohydrate supplementation and resistance training. J. Strength Cond. Res. 2003, 17, 187–196.
- Stephens FB, Chee C, Wall BJ, et al. Lipid-induced insulin resistance is associated with an impaired skeletal muscle protein synthetic response to amino acid ingestion in healthy young men. Diabetes. 2015;64:1615–20.
- Kimball SR, Ravi S, Gordon BS, Dennis MD, Jefferson LS. Amino acid-induced activation of mTORC1 in rat liver is attenuated by short-term consumption of a high-fat diet. J Nutri. 2015; 145(11):2496–2502.