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Muscle protein breakdown has a minor role in the protein anabolic response to essential amino acid and carbohydrate intake following resistance exercise
Author(s) -
Glynn Erin L,
Fry Christopher S,
Drummond Micah J,
Dreyer Hans C,
Dhanani Shaheen,
Volpi Elena,
Rasmussen Blake B
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.740.5
Subject(s) - anabolism , medicine , endocrinology , ingestion , chemistry , protein catabolism , carbohydrate , amino acid , catabolism , phenylalanine , biochemistry , biology , metabolism
Essential amino acid and carbohydrate (EAA+CHO) ingestion following resistance exercise (RE) enhances muscle protein synthesis (MPS). The purpose of this study was to determine if a reduction in MP breakdown (MPB) contributes to the enhanced protein anabolic response when EAA+CHO are ingested post‐RE. We hypothesized CHO‐induced insulin release would inhibit MPB resulting in augmented net muscle protein balance. Twelve male subjects were assigned to 2 groups containing equivalent amounts of EAA (~20g) but different amounts of CHO (EAA+30g CHO; EAA+90g CHO). Groups ingested the nutrients 1 hr after a bout of leg RE. Leg phenylalanine kinetics and associated signaling proteins were assessed on successive muscle biopsies using stable isotopic techniques and immunoblotting, respectively. MPB tended to decrease (P<0.1) and MPS increased (P<0.05) to a similar extent in both groups. Phosphorylation of AMPKα (Thr172) was elevated following RE and returned toward basal levels following drink ingestion only in EAA+90g CHO. Autophagy marker light chain 3B‐II significantly decreased following drink ingestion similarly in both groups (P<0.05). There were no changes in ubiquitin‐associated atrophy markers MuRF1 or MAFbx protein expression. We conclude the enhanced muscle protein anabolic response detected when EAA+CHO are ingested post‐RE is primarily (~70%) due to enhanced MPS with minor changes in MPB. Grant Funding Source : NIH/NIAMS RO1 AR049877 , NIH/NIA P30 AG024832 and NIH/NICHD T32 HD007539