In this study, sympathovagal modulation and interstitial glucose concentrations were for the first time recorded continuously and in parallel to assess the effects of exercise on the pre- and postprandial sequences of a spontaneously requested meal. Our results show, firstly, that in young male adults, exercise did not alter the preprandial sequence (delay, motivation to eat, preprandial glucose decline) but that under this condition the meal was requested in a metabolic state that was characterized by a higher proportion of energy being derived from fat. Secondly, the postprandial glucose response was increased in relative but not absolute values after exercise, and this was associated with an increase in fat oxidation and vagal withdrawal.
Exercise did not alter the motivation to eat or delay request for the meal. After a similar physical workload, exercise has been reported to reduce hunger ratings in some [23–25] but not all studies [26–31]. This effect was brief (<10 min) and no longer present at meal onset. Although these results were reported for a study with a similar number of subjects, the non-significant trend that we observed in the immediate post-exercise period for hunger and desire to eat suggests that a larger sample size may be required. While a slightly longer delay (5 min) until eating onset has been previously reported , this delay was not significantly changed in our study. Again, a higher number of subjects may be required in order to observe this effect. Therefore, specific research into this matter is needed in the future.
One of our hypotheses was that the glucose decline preceding a meal request would be altered by prior exercise. When an exercise that depleted muscle glycogen was performed on the day before testing, it has been reported that most meals were requested without a prior glucose decline . This was accompanied by a very low RER that was corrected after re-feeding. According to the criteria proposed by Melanson et al. [34, 35] that we adapted to be more conservative, a glucose decline was observed before 72% of lunch requests. In the other cases, glucose actually decreased during the preprandial interval, but the magnitude and duration of our modified criteria were not fulfilled. The mean delay between the onset of this preprandial glucose decline and the meal request was consistent with previous observations [33–35]. Exercise did not seem to impair this preprandial glucose profile since it was observed with a similar frequency in both conditions. However, our exercise was not designed to deplete muscle glycogen. Based on our glucose oxidation results (~ 146 g) and the energy partitioning proposed by Jeukendrup  (i.e., 80% of the glucose oxidized derived from glycogen) and the glucose oxidized at rest (~ 11 g), ~ 106 g of glycogen was used [(146 × 0.8) - 11]. According to the subjects' leg muscle mass, which was estimated at ~ 21 kg by the bioelectrical impedance analyzer, and a mean glycogen muscle concentration of 150 mmol/kg wet weight, it can be assumed that the exercise depleted glycogen of the whole leg muscle mass by only 18%. In our study, the RER also decreased after exercise when compared with the rest condition, but this did not prevent the occurrence of glucose declines. Therefore, it seems that the glycogen status, more than the exercise per se, is the reason behind the absence of a preprandial glucose decline, or more likely, the absence of its detection.
It must be noted that there was a much larger glucose decline at the onset of the exercise session (from ~ 5.0 to ~ 4.2 mmol.L-1), a well-known phenomenon mediated by the increase in muscle glucose uptake . This occurs despite the fact that liver potently increases its glucose output due to lower insulin and higher glucagon and catecholamine secretion . However, when preprandial glucose declines were observed, glucose concentrations were in a stable state in each subject.
Between the end of exercise and the meal request, carbohydrate oxidation was 46% lower than in the rest condition. Considering that ~ 20% of the CHO oxidized during exercise came from blood glucose , ~ 20 g of glucose needed to be compensated for, compared to the rest condition. Although the post-exercise reduction in glucose oxidation could not completely account for the compensation of this glucose difference, it may contribute to preclude an earlier preprandial glucose decline and meal request.
Glucose  and ghrelin  are the main putative determinants of meal initiation. We have previously reported that ghrelin is increased before meal request  but there are arguments against its role as a necessary factor in meal initiation . Moreover, ghrelin was not found to be altered after an exercise session of intensity and duration similar to the one used in our study . Cholecystokinin and glucagon-like peptide-1 have been reported to be increased after a single bout of exercise [11, 56, 57], but these hormones are involved in satiation or satiety and not in hunger.
Since the HRV indices were not different between conditions at the time subjects requested their meal, it seems that hunger occurs in a similar sympathovagal state after exercise or rest.
After exercise, the glucose peak was reached more than 30 min later than after rest. Since the rate of eating was kept similar across conditions, this may indicate that gastric emptying was slowed by prior exercise. The transit time of a 3331 kJ meal with 67% fat was not previously reported to be modified by prior exercise . However, mean energy intake at lunch in our study was higher (5225 ± 998 kJ), and the fat load was lower (45%) than in this previous study, so that this explanation cannot be excluded.
Based on the incremental profiles, exercise induced a higher postprandial glucose peak level and a 48% increase in total glucose response to the meal compared with the rest condition. Although our subjects were young and healthy, this could be interpreted as a detrimental effect of exercise since a sustained elevated postprandial glucose level is now considered an independent cardiovascular risk factor . However, the absolute values preclude such a conclusion because the glucose AUC over the 180 min was not different between conditions. These results suggest that this response might be explained by a lower basal glucose level after the exercise session, although it failed to reach statistical significance. It has been demonstrated that exercise consisting of a sufficient workload before a meal can induce a lower postprandial insulin level [5, 7, 13, 14]. This has been found to be partially explained by a reduced second-phase insulin secretion  and higher insulin clearance . Therefore, the exercise-induced increase in postprandial glucose response might be the result of reduced glucose transport into the muscles due to both lower insulin and a greater glucose output from the splanchnic region, which was facilitated by prior exercise . The increased post-exercise fatty oxidation observed in the muscle might also contribute to the increase in postprandial glucose. It has been documented that increasing fatty acid levels induces an increase in fat oxidation and decreased glucose oxidation via the inhibition of glucose transport/phosphorylation . The involvement of fat oxidation according to the well-known Randle cycle  has, to this day, only been demonstrated indirectly . That fat oxidation remained elevated by 46% in the exercise condition when compared to the rest condition 180 min after the meal supports this hypothesis. However, it is true that no study has yet demonstrated an increase in plasma glucose concentration due to an increase in fatty acid concentration. This absence has been attributed to a compensatory increase in insulin secretion , a phenomenon that might not occur following exercise.
Although increased heart rate indirectly suggests some sympathetic activation, the differences in LF/HF of the HRV analyses failed to reach significance. Interestingly, we actually observed that the previously described postprandial vagal withdrawal  was much more pronounced in the exercise than in the rest condition. The fact that this difference involved not only the HFms2 but also the HFnu suggests its vagal origin. Pancreatic β-cells express several G protein-coupled receptors that respond to parasympathetic innervation and in turn increase glucose-stimulated insulin secretion . Recently, the importance of vagal activity was demonstrated using atropine which partially blocked insulin sensitivity in the postprandial period . Thus, the effect of prior exercise on postprandial metabolism could involve postprandial vagal withdrawal and sympathetic activation, both of which would result in a transiently blunted glucose tolerance mediated by reduced insulin secretion [21, 66]. Importantly, this decrease in global HRV is not consecutive to a lower ability to detect variability . HRV is lower after exercise than after rest because exercise induces a significant decrease in parasympathetic activity and an increase in sympathetic activity (leading to the increased HR) but with a global diminution in global HRV . However, changes in vagal activity that are determined using HRV (i.e., heart branch) are not always associated with consistent changes in hormones, which are known to be highly dependent on the abdominal vagal activity . Therefore, this hypothesis requires further investigation.