During endurance exercise, skeletal muscle relies mainly on both carbohydrate (CHO) and fat oxidation to cover energy needs. Numerous scientific studies have shown that increasing the exercise intensity leads to a progressive utilization of CHO. The latter will induce a state of glycogen depletion which is generally recognized as being a limiting factor for the continuation of strenuous exercise. Different dietary interventions have been proposed to overcome this limitation. A high-CHO diet during periods of intense training and competition, as well as CHO intake during exercise, are known to maintain a high rate of CHO oxidation and to delay fatigue. However, it has been recognized also that enhancing fatty acid (FA) oxidation during exercise induces a reduced rate of glycogen degradation, resulting in an improved endurance capacity. This is most strikingly observed as a result of frequent endurance exercise which improves a number of factors known to govern the FA flux and the oxidative capacity of skeletal muscle. Such factors are: (1) blood flow and capillarization; (2) lipolysis of triacylglycerol (TAG) in adipose tissue and circulating TAG and transport of FA from blood plasma to the sarcoplasm; (3) availability and rate of hydrolysis of intramuscular TAG; (4) activation of the FA and transport across the mitochondrial membrane; (5) the activity of enzymes in the oxidative pathway; (6) hormonal adaptations, i.e. sensitivity to catecholamines and insulin. The observation that the plasma FA concentration is an important factor in determining the rate of FA oxidation, and that some dietary factors may influence the rate of FA supply to muscle as well as to the mitochondria, has led to a number of dietary interventions with the ultimate goal to enhance FA oxidation and endurance performance. It appears that experimental data are not equivocal that dietary interventions, such as a high-fat diet, medium-chain TAG-fat emulsions and caffeine intake during exercise, as well as L-carnitine supplementation, do significantly enhance FA oxidation during exercise. So far, only regular endurance exercise can be classified as successful in achieving adaptations which enhance FA mobilization and oxidation.

To study the effects of medium-chain triacylglycerols (MCT) on maternal lipid metabolism and pup growth, MCT (200 g/kg) were incorporated into a commercial chow diet and fed to lactating rats for 8–10 d. The results were compared with similar diets containing sunflower oil (polyunsaturated fatty acids; PUFA), tristearin (saturated fatty acid) or triolein (monounsaturated fatty acid). There was decreased food and energy intake with the MCT diet and this was accompanied by decreased (35%) pup growth. All the high-fat diets inhibited lipogenesis in vivo in the lactating mammary gland, the order of effectiveness being PUFA > triolein > tristearin > MCT. Only the MCT diet increased the rate of hepatic lipogenesis (180%). Experiments feeding an MCT meal containing [l-14C]octanoate indicated that very little (3–4%) of the C was present in mammary gland lipid, unlike the findings with [l-14C]triolein meal (40%). The major portion (65%) of the absorbed [l-I4C]octanoate was oxidized to 14CO2. There was no evidence for adaptation of the mammary gland to increased dietary lipid uptake on the triolein or MCT diets. It is concluded that the decreased pup growth on the MCT diet is due in part to the decreased energy intake and to the inability of dietary medium-chain fatty acids to provide substrates for milk lipid synthesis.

In order to study the rate of intestinal absorption and hepatic uptake of medium-chain fatty acids (MCFA), six growing pigs, mean body weight 65 kg, were fitted with a permanent fistula in the duodenum and with three catheters in the portal vein, carotid artery and hepatic vein respectively. Two electromagnetic flow probes were also set up, one around the portal vein and one around the hepatic artery. A mixture of octanoic and decanoic acids, esterified as medium-chain triacylglycerols, together with maltose dextrine and a nitrogenous fraction was continuously infused for 1 h into the duodenum. Samples of blood were withdrawn from the three vessels at regular intervals for 12 h and further analysed for their non-esterified octanoic and decanoic acid contents. The concentration of non-esterified octanoic and decanoic acids in the portal blood rose sharply after the beginning of each infusion and showed a biphasic time-course with two maximum values, one after 15 min and a later one between 75 and 90 min. Only 65 % of octanoic acid infused into the duodenum and 54 % of decanoic acid were recovered in the portal flow throughout each experiment. The amounts of non-esterified MCFA taken up per h by the liver were close to those absorbed from the gut via the portal vein within the same periods of time, showing that the liver is the main site of utilization of MCFA in pigs. These results have been discussed with a special emphasis laid on the possible mechanisms of the biphasic time-course of MCFA absorption and the incomplete recovery in the portal blood of the infused fatty acids.