Factors that increase fat oxidation can be important in both limiting fat accumulation and increasing loss of body fat stores. Repeated acute changes in fat oxidation resulting from fasting, feeding, and exercise can affect long-term fat balance and body fat stores. During a fasting, post-absorptive state, fatty acid oxidation contributes proportionately more to energy expenditure than does carbohydrate oxidation. This phenomenon is due largely to greater lipid and lower carbohydrate availability, as plasma non-esterified fatty acid (NEFA) concentrations rise in response to lower insulin and higher counter-regulatory hormone concentrations. On the other hand, consumption of a mixed meal (containing carbohydrate, fat and protein) increases blood insulin concentrations which in turn stimulates carbohydrate disposal and increases the contribution of carbohydrate oxidation to energy expenditure while suppressing lipolysis. Fat oxidation, then, decreases in the postprandial state compared to the period prior to meal consumption. The increased availability of postprandial glucose appears to also suppress fatty acid oxidation independent of the anti-lipolytic action of insulin, by inhibiting transport of long-chain fatty acids (LCFA) into the cellular mitochondria[2, 3]. Carbohydrate ingestion thus readily increases its own rate of oxidation. Conversely, adding fat to a carbohydrate-rich meal does not increase fat oxidation , although experimentally induced elevations of plasma NEFA using infused triacylglycerols can do so .
Vigorous acute exercise is characterized by hormonal changes that are opposite that of meal consumption. The rise in catecholamines suppresses pancreatic insulin secretion and increases lipolysis. Despite the increased rate of lipolysis, the mobilization of NEFAs from adipocytes during high intensity exercise may be compromised due to restricted blood flow to adipose tissue . However, during the early recovery period when insulin remains low, catecholamines remain elevated, and with increased blood flow to adipose tissue, plasma NEFA concentrations rise and fat oxidation is elevated [5, 6]. It is apparent then, that the hormonal milieu during the post-exercise period favors fat rather than carbohydrate oxidation. We have previously shown fat oxidation to be elevated following both strenuous endurance and resistance exercise [6, 7]. Elevations in plasma NEFAs have been shown to compromise glucose transport, as evidenced by infusion of lipids and heparin during hyperinsulinemic, euglycemic clamp studies , and it is possible that experimentally raising NEFAs via exercise could produce similar results.
It is not entirely clear what happens when meal consumption, which favors carbohydrate utilization, occurs during exercise recovery, a period which favors fat oxidation. It is possible that the resulting increase in circulating NEFAs could attenuate the ability of ingested carbohydrate to inhibit lipid oxidation. In studies supporting this notion, the contribution of fat oxidation to total energy expenditure was increased during 7-h , 10-h , and 17-h  post-exercise exercise time intervals, which included periods of feeding. For each of these studies, the exercise duration was substantial, lasting 3 hours.
Using a shorter exercise protocol (60 minutes, 50% of VO2 max, with a net energy cost of approximately 600 kcal) Dionne et al  reported no differences in substrate oxidation over a 24 hour period in which subjects were kept in energy balance, whether they exercised or not. Votruba et al , found prior exercise (300 kcal) compared to a no exercise condition produced a sustained increase in oleate oxidation in recovery in response to ingestion of labeled oleate. However, when labeled palmitate was administered, post-exercise palmitate oxidation was not increased relative to the no-exercise trial. It remains unclear what is the effect on substrate oxidation of increasing carbohydrate availability by providing a meal immediately following exercise of the intensity and duration often advocated for health-related fitness (i.e. 60–70% VO2peak for 30–60 minutes). Therefore, we determined whether an acute bout of endurance exercise would attenuate the rapid decrease in fat oxidation that normally follows ingestion of a carbohydrate-rich meal. For this study, we used a portion of the data from a previously published study on the effect of prior exercise on the glycemic index , and added an additional treatment condition and used the changes in plasma NEFAs and fat oxidation as endpoints, which were not a part of the previous study.