Activity energy expenditure is a major determinant of dietary fat oxidation and trafficking, but the deleterious effect of detraining is more marked than the beneficial effect of training at current recommendations

Background: Previous studies suggested that physical activity energy expenditure (AEE) is a major determinant of dietary fat oxidation, which is a central component of fat metabolism and body weight regulation. Objective: We tested this hypothesis by investigating the effect of contrasted physical activity levels on dietary saturated and monounsaturated fatty acid oxidation in relation to insulin sensitivity while controlling energy balance. Design: Sedentary lean men (n = 10) trained for 2 mo according to the current guidelines on physical activity, and active lean men (n = 9) detrained for 1 mo by reducing structured and spontaneous activity. Dietary [d(31)]palmitate and [1-C-13]oleate oxidation and incorporation into triglyceride-rich lipoproteins and nonesterified fatty acid, AEE, and muscle markers were studied before and after interventions. Results: Training increased pahnitate and oleate oxidation by 27% and 20%, respectively, whereas detraining reduced them by 31% and 13%, respectively (P < 0.05 for all). Changes in AEE were positively correlated with changes in oleate (R-2 = 0.62, P < 0.001) and palmitate (R-2 = 0.66, P < 0.0001) oxidation. The d(31)-palmitate appearance in nonesterified fatty acid and very-low-density lipoprotein pools was negatively associated with changes in fatty acid translocase CD36 (R-2 = 0.30), fatty acid transport protein 1 (R-2 = 0.24), and AcylCoA synthetase long chain family member 1 (ACSL1) (R-2 = 0.25) expressions and with changes in fatty acid binding protein expression (R-2 = 0.33). The d(31)-palmitate oxidation correlated with changes in ACSL1 (R-2 = 0.39) and carnitine palmitoyltransferase 1 (R2 = 0.30) expressions (P < 0.05 for all). Similar relations were observed with oleate. Insulin response was associated with AEE (R-2 = 0.34, P = 0.02) and oleate (R-2 = 0.52, P < 0.01) and palmitate (R-2 = 0.62, P < 001) oxidation. Conclusion: Training and detraining modified the oxidation of the 2 most common dietary fats, likely through a better trafficking and uptake by the muscle, which was negatively associated with whole-body insulin sensitivity.