Coronary heart disease (CHD) is the main cause of mortality amongst adults in the U.S. Plasma hypertriglyceridaemia, an independent risk factor for CHD, is more prevalent in older adults, making older adults an at-risk group for CHD. Amino acid (AA) intake has been shown to lower both hepatic and plasma triglyceride (TG) concentrations in older adults (Børsheim et al., 2009). We have also shown that acute AA intake increases hepatic very low density lipoprotein (VLDL) TG and apolipoprotein B-100 secretion (Børsheim et al., in preparation). Furthermore, very recent data from our group have shown that 13CO2 breath enrichment, measured during a constant infusion of U-13C16-palmitate, is increased with AA intake relative to a basal period (Hurren et al., in progress). Collectively, our observations suggest that acute AA intake increases hepatic TG secretion while seemingly increasing fatty acid (FA) uptake and oxidation, presumably within skeletal muscle. However, whether this apparent increase in FA oxidation is the result of altered skeletal muscle mitochondrial function is not known. Here we investigated the impact of acute AA intake on skeletal muscle mitochondrial function in older adults. Five older adults (mean±SD: 63.3±7.8 years) with elevated plasma TG concentrations (2.16±0.95 mmol/l) participated in this study. Skeletal muscle biopsies were obtained before and after acute AA intake (21g of AAs in total: 1g ingested every 10 minutes for 3.5h). Mitochondrial function was assessed in permeabilised myofibres with the sequential addition of pyruvate (5mM), malate (2mM), glutamate (5mM), palmitoyl-carnitine (150µM), ADP (5mM) and succinate (10mM). VO2 values were normalized to citrate synthase (CS) protein content. State 3 (ADP-dependant) respiration was not different following AA intake (mean±SEM: 0.74±0.04 vs 0.66±0.09 pmol/(sec*mg)/µg CS, figure 1). The ability of the mitochondria to oxidise the FA palmitate (palmitoyl-carnitine) did not change following AA acid intake (0.76±0.04 vs 0.74±0.09 pmol/(sec*mg)/µg CS, figure 1). In addition, maximal mitochondrial oxidative respiration determined following the addition of succinate was not altered by AA acid intake (1.09±0.04 vs. 1.12±0.09 pmol/(sec*mg)/µg CS, figure 1). Here we provide evidence that acute AA intake does not alter skeletal muscle mitochondrial function in older adults. Apparent changes in palmitate oxidation following acute AA intake are therefore likely to be the result of increased intracellular FA availability and oxidation in vivo. However, whether long-term AA supplementation alters mitochondrial function in older adults warrants investigation.