Lower glycemic and insulinemic responses were observed when two daily LGI meals were consumed for 5 consecutive days compared to the consumption two daily HGI meals for this same period of time. However, these responses did not differ according to GI during exercise. There was a lower level of fat oxidation in the 90 minutes pre-exercise after the ingestion of the LGI meal than there was after the ingestion of the HGI meal. GI did not affect free fatty acids levels before and during exercise. Lactate concentration during exercise was also not affected by the study treatments.
It has been suggested that the ingestion of LGI foods, compared to HGI foods, results in lower and more stable glucose and insulin levels [3, 4, 6]. However, the consumption of breakfast cereals differing in GI did not lead to differences in the areas under the insulinemic response curves between the LGI and HGI groups in our study. In one prior study, the lower GI seen after consumption of bran cereal was attributed to an earlier postprandial hyperinsulinemia, which attenuated the increase in the plasma glucose concentration . However, the bran cereal in that study had almost 4 times more protein than the corn flakes (high GI cereal) . It has been demonstrated that the addition of protein to a meal increases insulin secretion, leading to a reduction in the GI of that meal [19, 35].
In the present study, the test meals had the same protein content. The highest glycemic response was reached 30 min after the consumption of the HGI and the LGI meals. HGI glycemic levels from 60-120 min were significantly lower than the peak level. However, these levels were not lower than the baseline level (fasting condition). LGI glycemic response was stable during the 60-120 min period.
Ingestion of the LGI meal did not affect the glycemic response during the postprandial period and during exercise . Although the glycemic response observed in the first day did not vary significantly, the consumption of the LGI meal for five consecutive days led to a significantly higher glycemia at 30 min than at 60 min. This result suggests that although the short-term glycemic response to the LGI meal may lead to stable glycemia, this type of response may not be maintained when LGI foods are ingested for several consecutive days. The mechanism responsible for the change in the observed glycemic response pattern should be investigated in future studies.
According to some authors, the lower and more stable glucose levels observed after the consumption of LGI foods (versus HGI foods) is important to maintaining an adequate concentration of glucose for use as an energy source during exercise [4, 6]. In the present study, the 30-90 min IR was significantly higher after consumption of the HGI than after consumption of the LGI meal. However, there was no difference in this type of response during exercise. Similar responses were verified in other studies in which foods differing in GI were consumed before cycling in a cyclo ergometer at 70% of VO2 max [8, 9, 16].
There was no effect of test meals GI on free fatty acid concentrations during the 120 min in which this parameter was evaluated. However, in two other studies [5, 15] there were lower free fatty acid concentrations during the 180 min after the consumption of a LGI meal compared to a HGI meal. However, fructose was not an ingredient in the test foods in these last two studies mentioned [5, 15], whereas fructose was included in the LGI meals in our study.
Fructose decreases insulin secretion  and is rapidly taken up independently of insulin, primarily in liver cells, where it is quickly metabolized to triose-phosphates, which can be oxidized or released as lactate . Due to its ability to reduce insulin secretion, fructose down-regulates lipoprotein lipase (LPL) activity . LPL is a central enzyme of lipid metabolism, which catalyzes the hydrolysis of triglycerides, producing free fatty acids and glycerol . Therefore, the presence of fructose in the LGI meal in this study favored the lower IR observed, which, in turn, may have reduced LPL activity, leading to a reduction in triglycerides hydrolysis and therefore in the release of free fatty acids.
However, the concentrations of free fatty acids after the consumption of HGI meals in the present study were similar to those observed in other studies [6, 9, 15]. In all these studies, the postprandial (before and during exercise) fatty acid levels did not change significantly with time. However, these levels were lower than the levels measured during the fasting condition. These responses were possibly due to the higher glycemic response and IR observed in this study, as well as the higher carbohydrate oxidation rate seen after the ingestion of the HGI meal than when subjects were fasting.
In the present study, as well as in others [4, 6], lactate levels during exercise were not affected by GI. Diets differing in GI, when consumed before exercise by recreational athletes, did not affect the lactate concentration during a 60 min exercise at 65% of VO2 max  or 70% of VO2 max . Therefore, the results of these studies indicate that lactate concentrations are not affected by GI in active subjects.
The results obtained in the present study and in two other studies [6, 40] indicate that the ingestion of high carbohydrate meals increases the levels of carbohydrate oxidation compared to the fasting state, independently of the GI of the meal consumed. In the present study, there was a lower fat oxidation and a higher carbohydrate oxidation in the 90 min period following the ingestion of the LGI meal than there was with the HGI meal.
However, an earlier study  reported a 118% increase in fat oxidation during the first 80 min of exercise associated with the consumption of LGI foods compared with the consumption of HGI foods. In a more recent study  conducted by these same authors, it was shown that during exercise at 70% of VO2 max conducted for 30 min by recreational runners, there was more fat oxidation after the ingestion of LGI foods than after the ingestion of HGI foods. Although fat oxidation was not affected by the GI of test foods consumed prior to exercise in that study , the consumption of an LGI diet 3 h before exercise at 65% of VO2 max did not affect fat oxidation before the exercise . In contrast, the consumption of HGI diets, resulted in higher carbohydrate oxidation during a 2-hour period of exercise at 70% of VO2max [9, 16]. The results of these studies suggest that while substrate oxidation is not affected by GI of test meals consumed prior to exercise, the consumption of a LGI diet resulted in an increase in fat oxidation during exercise [5, 6, 16].
However, the lower fat oxidation observed in the present study could reflect the way in which fructose affects the oxidation of substrates. Other investigators showed that the ingestion of 50 g of fructose (LGI) caused a higher carbohydrate oxidation and a lower fat oxidation than when the same amount of glucose (HGI) was consumed . This indicates that the consumption of LGI meals containing less fructose (21.3 ± 1.83 g in the present study) may also result in this same substrate oxidation profile.
Fructose metabolism occurs mainly in the liver. This carbohydrate rapidly enters the cells through GLUT 2, without any energy cost or insulin requirement. Once inside the cells, fructose is rapidly converted into fructose-1-phosphate, which can then lead to the formation of fructose-1, 6-bisphosphate. This substrate can, in turn, be converted into glucose, acting as a primary glycolysis and oxidative phosphorylation supplier (carbohydrate oxidation) .
Nevertheless, in another study the consumption of a low GI test meal containing about the same amount of fructose (0.37 g/kg of body weight) as used in this study (0.32 g/kg of body weight) prior to running on a motorised treadmill resulted in similar level of fat oxidation compared with the high GI meal . Factors contributing to the differences between that study  and the present study are not well understood and should be investigated in future studies.
It has been shown that fructose consumption results in an influx of carbohydrates into cells, increasing glycolysis and mitochondrial citrate synthesis. The subsequent increase in malonyl coenzyme A inhibits the activity of carnitine palmitoyltransferase 1, which transports fatty acids into mitochondria, leading to a reduction in fat oxidation . Therefore, the results of the present study suggests that the consumption of fructose 90 minutes before a competition may not be recommended because fructose favors a higher carbohydrate oxidation, which can, in turn, lead to a reduction in glycogen storage, potentially compromising the main energy substrate used during exercise.
Compared with the HGI session, during the LGI session (fructose ingestion), there was a higher respiratory exchange ratio during the DIT assessment. This result is the opposite of the results reported in two other studies [5, 6]. However, in the present study and in the study by Wu et al. (2003) , the respiratory exchange ratio during fasting was lower than the respiratory exchange ratios after the consumption of the HGI and LGI meals. These results suggest that, compared with the fasting condition, there was an increase in postprandial carbohydrate oxidation, which was not dependent on the GI of the ingested meal.
The energy expenditure after the consumption of HGI and LGI meals on days 1 and 5 of each session was higher than that in the fasting condition. A similar response was observed after the consumption of 75 g of different sources of carbohydrate . Such effects reflect the increase in energy expenditure for digestion , absorption , metabolism, and storage of the consumed nutrients, as a result of the DIT . According to Westerterp (2004) , carbohydrates are responsible for 5-10% of the energy expenditure from DIT. However, the DIT was not affected by the GI of the test meals in the present study.
In contrast, in another study  the consumption of 25 g of xylitol (GI = 7) did not modify significantly the energy expenditure in the 60-120 min postprandial when compared with the fasting condition. However, the ingestion of 25 g of glucose (GI = 100) led to an energy expenditure that was significantly higher than that at baseline. According to the authors of that study, although these sugars were consumed in isocaloric portions, xylitol enters the cells independently of insulin action and is slowly converted to glucose-6-phosphate. Xylitol does not affect fat and/or carbohydrate oxidation. All D-glucose derived from xylitol metabolism is primary stored as glycogen in the liver, which is then gradually released into the blood stream as glucose .