Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation Stephen P. Bird 4 , Kyle M. Tarpenning, Frank E. Marino School of Human Movement Studies, Charles Sturt University, Bathurst, NSW 2795, Australia Received 13 June 2005; accepted 15 November 2005 In memory of the late Dr Kyle Tarpenning. Abstract A number of physiological events including the level of contractile activity, nutrient status, and hormonal action influence the magnitude of exercise-induced skeletal muscle growth. However, it is not the independent action of a single mechanism, but the complex interaction between events that enhance the long-term adaptations to resistance training. The purpose of the present investigation was to examine the influence of liquid carbohydrate (CHO) and essential amino acid (EAA) ingestion during resistance exercise and modification of the immediate hormonal response on myofibrillar protein degradation as assessed by 3-methylhistidine (3-MH) excretion. After a 4-hour fast, 32 untrained young men (18-29 years) performed a single bout of resistance exercise (complete body; 3 sets  10 repetitions at 75% of 1-repetition maximum; 1-minute rest between sets), during which they consumed a 6% CHO (n = 8) solution, a 6-g EAA (n = 8) mixture, a combined CHO + EAA (n = 8) supplement, or placebo (PLA; n = 8) beverage. Resistance exercise performed in conjunction with CHO and CHO + EAA ingestion resulted in significantly elevated ( P b .001) glucose and insulin concentrations above baseline, whereas EAA ingestion only increased the postexercise insulin response ( P b .05). Time matched at 60 minutes, the PLA group exhibited a peak cortisol increase of 105% ( P b .001) with no significant change in glucose or insulin concentrations. Conversely, the CHO and CHO + EAA groups displayed a decrease in cortisol levels of 11% and 7%, respectively. Coinciding with these hormonal response patterns were significant differences in myofibrillar protein degradation. Ingestion of the EAA and CHO treatments attenuated 3-MH excretion 48 hours after the exercise bout. Moreover, this response was synergistically potentiated when the 2 treatments were combined, with CHO + EAA ingestion resulting in a 27% reduction ( P b .01) in 3-MH excretion. In contrast, the PLA group displayed a 56% increase ( P b .01) in 3-MH excretion. These data demonstrate that not only does CHO and EAA ingestion during the exercise bout suppress exercise-induced cortisol release; the stimulatory effect of resistance exercise on myofibrillar protein degradation can be attenuated, most dramatically when the treatments are combined (CHO + EAA). Through an banticatabolic effect,Q this altered balance may better favor the conservation of myofibrillar protein. D 2006 Elsevier Inc. All rights reserved. 1. Introduction Resistance exercise stimulates immediate changes in the rate of muscle protein turnover, resulting in an increase in both protein synthesis and protein degradation [1-3]. Any imbalance between the rate of protein synthesis and rate of protein degradation will lead to a change in the size of the protein tissue pool [4]. Thus, for protein accretion to occur, the rate of synthesis must exceed the rate of degradation. However, in the absence of nutritional intake, net muscle protein balance (ie, the difference between protein synthesis and protein degradation) remains negative in the early stages of recovery [2]. A number of studies support the notion that hormonal events play critical roles in controlling protein turnover [5-7], with the response of insulin and cortisol receiving much attention, as they are intimately involved in this cyclical process. Although the ability to alter the anabolic hormonal milieu and the influence that such adjustments have on modifying protein synthesis are well documented [8-10], the ability to alter the catabolic hormonal environment and the impact that such a change might have on affecting protein degradation have received considerably less attention. 0026-0495/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2005.11.011 4 Corresponding author. Tel.: +61 612 6338 4155; fax: +61 612 6338 4065. E-mail address: sbird@csu.edu.au (S.P. Bird). Metabolism Clinical and Experimental 55 (2006) 570 – 577 www.elsevier.com/locate/metabol