Bergouignan A, Schoeller DA, Votruba S, Simon C, Blanc S. The acetate recovery factor to correct tracer-derived dietary fat oxidation in humans. Am J Physiol Endocrinol Metab 294: E645-E653, 2008. First published January 22, 2008 doi:10.1152/ajpendo.00720.2007.-When using 13 C tracer to measure plasma fat oxidation, an acetate recovery factor should be determined in every subject to correct for label sequestration. Less is known regarding the acetate recovery factor for dietary fatty acid oxidation. We compiled data from six studies to investigate the determinants of the dietary acetate recovery factor (dARF) at rest and after physical activity interventions and compared the effects of different methods of dARF calculation on both the fat oxidation and its variability. In healthy lean subjects, dARF was 50.6 Ϯ 5.4% dose (n ϭ 56) with an interindividual coefficient of variation of 10.6% at rest and 9.2% after physical activity modifications. The physical activity interventions did not impact dARF, and the intraindividual coefficient of variation was 4.6%. No major anthropological or physiological determinants were detected except for resting metabolic rate, which explains 7.4% of the dARF variability. Applying an individual or an average group dARF did not affect the mean and the variability of the derived dietary lipid oxidation at rest or after physical activity interventions. Using a mean dARF for a group leads to over-or underestimation of fat oxidation of less than 10% in individual subjects. Moreover, the use of a group or individual correction did not affect the significant relationship found between fasting respiratory exchange ratio and dietary fat oxidation. These data indicate that an average dARF can be applied for longitudinal and cross-sectional studies investigating dietary lipid metabolism. exogenous fatty acid oxidation; stable isotopes; mass spectrometry STABLE ISOTOPES ARE EMPLOYED in clinical nutrition studies to measure fatty acid oxidation. The rate of excretion of labeled CO 2 following a constant infusion or ingestion of 13 C-labeled fatty acids is used to measure the tracer oxidized (2, 5, 6, 11). However, early studies (3) showed that the appearance of 13 CO 2 in breath is very low in the first hours of infusion, especially at rest. This finding suggested that part of the labeled carbon is temporarily sequestrated in the organism due to label dilution and/or redistribution, resulting in an underestimation of the tracer fat oxidation rates. Although dilution occurs mainly in the bicarbonate pool (4, 7), Wolfe and Jahoor (22) reported that the main sequestration of labeled carbon actually occurs in the TCA cycle. Indeed, labeled carbons were found in glutamate and glutamine and in lower quantity in glucose and lactate and pyruvate (15). On the basis of the observation that acetate is converted into acetyl-CoA and directly enters the TCA cycle, Sidossis et al. (14) were the first to propose that infused [ 14 C]acetate can be used to correct for the retention of a 13 C-fatty acid ( 13 C-FA...