The post-exercise period is often considered the most critical part of nutrient timing. An intense resistance training workout results in the depletion of a significant proportion of stored fuels (including glycogen and amino acids) as well as causing damage to muscle fibers. Theoretically, consuming the proper ratio of nutrients during this time not only initiates the rebuilding of damaged tissue and restoration of energy reserves, but it does so in a supercompensated fashion that enhances both body composition and exercise performance. Several researchers have made reference check details to an “anabolic

window of opportunity” whereby a limited time exists after training to optimize training-related muscular adaptations [3–5]. However, the importance – and even the existence – of a post-exercise ‘window’ can vary according to a number of factors. Not only is nutrient timing research open to question in terms of applicability, but recent evidence has directly challenged the classical view of the relevance of post-exercise nutritional intake on anabolism. Therefore, the purpose of this paper will be twofold: 1) to review the existing literature on the effects of nutrient

timing with respect to post-exercise muscular adaptations, and; 2) to draw relevant conclusions that allow evidence-based nutritional recommendations to be made for maximizing the anabolic response to exercise. Glycogen repletion A primary goal of traditional post-workout Selleck HDAC inhibitor PD184352 (CI-1040) nutrient timing recommendations is to replenish glycogen stores. Glycogen is considered essential to optimal resistance training performance, with as much as 80% of ATP production during such training derived from glycolysis [6]. MacDougall et al. [7] demonstrated that a single set of elbow flexion at 80% of 1 repetition maximum (RM) performed to muscular failure caused a 12% reduction in mixed-muscle glycogen concentration, while three sets at this intensity resulted in a 24% decrease. Similarly, Robergs et al. [8] reported that 3 sets of 12 RM performed to muscular

failure resulted in a 26.1% reduction of glycogen stores in the vastus lateralis while six sets at this intensity led to a 38% decrease, primarily resulting from glycogen depletion in type II PARP activation fibers compared to type I fibers. It therefore stands to reason that typical high volume bodybuilding-style workouts involving multiple exercises and sets for the same muscle group would deplete the majority of local glycogen stores. In addition, there is evidence that glycogen serves to mediate intracellular signaling. This appears to be due, at least in part, to its negative regulatory effects on AMP-activated protein kinase (AMPK). Muscle anabolism and catabolism are regulated by a complex cascade of signaling pathways.