Protein-rich food ingestion stimulates mitochondrial protein synthesis in sedentary young adults of different BMIs

Context: Excess fat mass may diminish the anabolic potency of protein-rich food ingestion to stimulate muscle protein subfractional synthetic responses. However, the impact of adiposity on mitochondrial protein synthesis (MPS) rates after protein-rich food ingestion has not been thoroughly examined in vivo in humans. Objective: We compared basal and postprandial MPS and markers of muscle inflammation [toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein 88 (MyD88) protein content] in young adults with different body mass indices (BMIs). Methods: Ten normal-weight (NW; BMI = 22.7 6 0.4 kg/m2), 10 overweight (OW; BMI = 27.1 6 0.5 kg/m2), and 10 obese (OB; BMI = 35.9 6 1.3 kg/m2) adults received primed continuous L-[ring-13C6]phenylalanine infusions, blood sampling, and skeletal muscle biopsies before and after the ingestion of 170 g of pork. Results: Pork ingestion increased muscle TLR4 and MyD88 protein content in the OB group (P , 0.05), but not in the NW or OW groups. Basal MPS was similar between groups (P . 0.05). Pork ingestion stimulated MPS (P , 0.001; 0 to 300 minutes) in the NW (2.5- 6 0.6-fold above baseline values), OW (1.7- 6 0.3-fold), and OB groups (2.4- 6 0.5-fold) with no group differences (P . 0.05). Conclusions: Protein-dense food ingestion promotes muscle inflammatory signaling only in OB adults. However, the consumption of a dinner-sized amount of protein strongly stimulated a postprandial MPS response irrespective of BMI. Our data suggest that alterations in postprandial MPS are unlikely to contribute to compromised muscle macronutrient metabolism witnessed with obesity.