The effects of carbohydrate and amino acids on muscle protein synthesis after acute resistance exercise and muscle adaptation following chronic resistance training
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Resistance exercise (RE) is purported to induce muscle protein accretion primarily by stimulating muscle protein synthesis (MPS), with its effect potentiated by providing a protein or amino acid (AA) supplement post exercise. Glutamine, a conditionally essential AA, is increasingly recommended to improve exercise performance, but it is poorly soluble and unstable in sports drinks. This limitation can be overcome by combining L-glutamine with L-alanine to form a dipeptide (AlaGln). The first study demonstrated that AlaGln supplementation post resistance exercise significantly reduced the phosphorylation of AMPK and NF-kB p65 without activating intracellular signals for MPS. This study also showed that whey protein (WP) activated the mTOR signaling pathways without affecting signaling proteins that controls muscle protein breakdown (MPB). The results provide indirect evidence that AlaGln blocks MPB via suppressing the activation of AMPK-FOXO3A and NF-kB p65, while WP promotes MPS. Recent research suggests that adding carbohydrate (CHO) to a protein supplement post exercise can produce greater protein accretion and subsequently increase the magnitude of resistance training adaptation relative to protein supplementation alone. Early studies from our laboratory found that co-ingestion of CHO and protein, as compared with CHO or protein intake individually, had a greater effect on the activation of anabolic signaling proteins. However, the effect of CHO plus protein on MPS and muscle adaptation is controversial. The second study demonstrated that adding CHO to a protein supplement (CP) accelerated MPS via activating the mTOR-signaling pathway in comparison with placebo (PLA) and WP during early exercise recovery, but CP did not affect signaling proteins that regulate MPB. The third study found that CP enhanced muscle strength relative to PLA and WP. The greater strength development in CP appeared due to increased myofibrillar protein content. Increased muscle hypertrophy occurred without an increase in myonuclei suggesting satellite cell activation was not required for muscle fiber development. Taken together, the results of this series of studies suggest that 1) AlaGln inhibits MPB following acute RE; 2) Adding CHO to a protein supplement accelerates muscle recovery by stimulating MPS, and increases the magnitude of muscle strength by accumulating more myofibrillar protein in comparison with PLA and WP.