Endurance training has been shown to increase fat oxidation both at rest and during exercise. However, most exercise training studies have been performed at high exercise intensity in well-trained athletes, and not much is known about the effect of a low-intensity training program on fat oxidation capacity in lean sedentary humans. Here, we examine the effect of 3-month lowintensity training program on total and intramuscular triglyceride (IMTG)-and/or VLDL-derived fat oxidation capacity and skeletal muscle mRNA expression. Six healthy untrained subjects (aged 43 ؎ 2 years, BMI 22.7 ؎ 1.1 kg/m 2 , VO 2max 3.2 ؎ 0.2 l/min) participated in a supervised 12-week training program at 40% VO 2max three times weekly. Total and plasma-derived fatty acid oxidation at rest and during 1 h exercise was measured using [13 C]palmitate, and in a separate test, [ 13 C]acetate recovery was determined. Muscle biopsies were taken after an overnight fast. Total fat oxidation during exercise increased from 1,241 ؎ 93 to 1,591 ؎ 130 mol/min (P ‫؍‬ 0.06), and IMTG-and/or VLDL-derived fatty acid oxidation increased from 236 ؎ 84 to 639 ؎ 172 mol/min (P ‫؍‬ 0.09). Acetyl-CoA carboxylase-2 mRNA expression was significantly decreased after training (P ‫؍‬ 0.005), whereas lipoprotein lipase mRNA expression tended to increase (P ‫؍‬ 0.07). In conclusion, a minimal amount of physical activity tends to increase fat oxidation and leads to marked changes in the expression of genes encoding for key enzymes in fat metabolism. Diabetes 51:2220 -2226, 2002

The validity of estimations of plasma fatty acid oxidation using tracers has often been questioned. The appearance of isotopic markers in breath CO2 is delayed and incomplete. Recently suggestions have been made that substantial amounts of tracer are incorporated into products of the tricarboxylic acid cycle (e.g. glucose, glutamine and glutamate) and that an acetate correction factor can be used to correct for tracer fixation. In the present study we investigated whether the appearance of 13CO2 during a separate infusion of [1,2‐13C]acetate could be used for correction of [U‐13C]palmitate oxidation rates in studies lasting <2 h and we quantified the appearance of tracer in the glutamine, glutamate and glucose pools of the body. An infusion of either [1,2‐13C]acetate (0.104 μmol min−1 kg−1) or [U‐13C]palmitate (0.013 μmol min−1 kg−1) was given to eight male subjects and continued for 2 h at rest. In six subjects the infusion of [1,2‐13C]acetate was repeated to determine reproducibility of the acetate recovery. Fractional recovery in breath from [1,2‐13C]acetate gradually increased during the infusion period at rest from 14.1 ± 0.6 % at 60 min to 26.5 ± 0.5 % at 120 min after the start of the infusion. Intersubject coefficient of variance was 8.3 ± 0.6 % and intrasubject coefficient of variance of the acetate recovery tests was 4.0 ± 1.5 %. After 2 h of [1,2‐13C]acetate infusion, 12.4 ± 0.8 and 10.3 ± 0.9 % of infused 13C was incorporated in the glutamine and glutamate pools, respectively. In conclusion, the [1,2‐13C]acetate recovery factor can be used for correcting the rate of [U‐13C]palmitate oxidation in infusing studies of 2 h in resting conditions. Failure to use this recovery factor leads to a substantial underestimation of the rate of plasma free fatty acid oxidation. The extent of label fixation could largely be explained by accumulation of tracer carbon in glutamine and glutamate, and the accumulation in glucose is negligible.

. Effect of exercise training at different intensities on fat metabolism of obese men. J Appl Physiol 92: 1300-1309, 2002; 10.1152/japplphysiol.00030.2001.-The present study investigated the effect of exercise training at different intensities on fat oxidation in obese men. Twenty-four healthy male obese subjects were randomly divided in either a low-[40% maximal oxygen consumption (V O2 max)] or high-intensity exercise training program (70% V O2 max) for 12 wk, or a nonexercising control group. Before and after the intervention, measurements of fat metabolism at rest and during exercise were performed by using indirect calorimetry, [U-13 C]palmitate, and [1,2-13 C]acetate. Furthermore, body composition and maximal aerobic capacity were measured. Total fat oxidation did not change at rest in any group. During exercise, after low-intensity exercise training, fat oxidation was increased by 40% (P Ͻ 0.05) because of an increased non-plasma fatty acid oxidation (P Ͻ 0.05). Highintensity exercise training did not affect total fat oxidation during exercise. Changes in fat oxidation were not significantly different among groups. It was concluded that lowintensity exercise training in obese subjects seemed to increase fat oxidation during exercise but not at rest. No effect of high-intensity exercise training on fat oxidation could be shown. low intensity; stable isotopes; acetate correction factor; [ 13 C]palmitate OBESITY IS ASSOCIATED with an impaired ability to use fat as a fuel. This may contribute to the development and maintenance of large fat stores. Upper body obesity is associated with an impaired postabsorptive free fatty acid (FFA) utilization in skeletal muscle in women (6). Isoprenaline-induced fat oxidation and skeletal muscle FFA uptake are impaired in obese men, and no improvement was found after weight loss (1-3). Lean, formerly obese women have lower fasting fat oxidation rates compared with lean, never-obese women (32). Moreover, in Pima Indians, a population with a high prevalence of obesity, weight gain is association with a low 24-h fat-to-carbohydrate oxidation ratio (49). Several explanations have been proposed for this reduced fat utilization in obesity, such as a low activity of enzymes of ␤-oxidation (50), low skeletal muscle lipoprotein lipase activity (7), and impaired mobilization of fat stores (1). Interventions that will increase the capacity of the skeletal muscle to utilize fat may, therefore, make an important contribution to weight management in obese individuals and individuals at risk for obesity.Endurance exercise training is known to increase fat oxidation during submaximal exercise at a fixed workload in lean subjects (14,17,23,30,38). Cross-sectional studies also report higher fat oxidation during exercise after an overnight fast (18,20,21,40,45) or with glucose (19, 47) in trained compared with sedentary men. Some studies also found an enhanced resting fat oxidation after endurance training (5, 31, 34). Thus endurance exercise training appears to have the capacity to increase ...

Addition of low-intensity exercise training to energy restriction counteracts the decline in fat oxidation during the postdiet period.

Objective: To investigate the effect of dietary restraint with or without exercise during weight maintenance after energy restriction. Subjects and methods: In total, 40 obese male subjects (mean BMI 32.3 kg/m 2 ; mean age 39 y) were recruited and randomly divided into a diet (D; n ¼ 20) and a diet plus exercise (DE; n ¼ 20) group. Both groups participated in an energy restriction programme (ER), which was followed by a weight maintenance phase (WM). Subjects in the DE also participated in an exercise programme. Body mass (BM) and the scores on the three factor eating questionnaire (TFEQ) were measured before and after the ER and after WM. Results: No significant differences between both groups were found. All data taken together showed that BM loss during ER was explained by initial BM (r 2 ¼ 0.3, Po0.0005) and inversely by initial cognitive restraint (F1) (r 2 ¼ 0.4, Po0.0005) in a stepwise regression. BM regain during WM was explained by BM loss (r 2 ¼ 0.5, Po0.001) and by increase in F1 during ER (r 2 ¼ 0.6, Po0.001), while the exercise intervention did not contribute further to the explained variation. Subjects with a relatively high diet frequency prior to the study had relatively significant higher initial F1 scores (Po0.05). During ER, increase in F1 was associated with decrease in general hunger (F3). Conclusion: Successful BM loss was associated with higher initial BM and lower initial F1. Successful WM was explained by BM loss and increase in F1 during ER, irrespective of possible exercise training effects. Successful WM was reduced when F1 scores reach their limit, due to diet-frequency.