DISCUSSION
obese, fatty liver diseases, SIT, high‐intensity, diabetes
OBESE, CVD, DYSLIPIDEMIA, HYPERTENSION, DIABETES
In the present study, we aimed to explore the effects of acute SIT on metabolic response and substrate utilization after an oral 75‐gram glucose load in individuals with overweight/obesity. We found that the fat contribution to energy expenditure and lactate levels significantly increased during the postprandial period after SIT, whereas the carbohydrate contribution was reduced. Moreover, the fat contribution and lactate concentration AUC were significantly higher in the SIT group than in the resting group, whereas the carbohydrate contribution AUC was lower. Furthermore, the RQ was lower in the SIT group than in the resting group at 120 min of the postprandial period and the RQ AUC was also lower in the SIT group. These results indicate that acute SIT may have positive effects on the metabolic response to postprandial glucose in adults with overweight/obesity.Exercise is well‐documented to increase fat oxidation, which is principally due to the decrease of re‐esterification (Ho et al., In addition to fats, it is known that carbohydrates are simultaneously oxidized during energy production (Spriet, Regarding RQ, which reflects substrate utilization when energy is expended, we found that while this metric increased at 60 min after a glucose load, it was significantly lower in the SIT group than in the control group at 120 min postprandial. Our findings confirm prior observations of differential RQ responses to exercise training, with high‐intensity exercise shown induce a greater reduction in RQ (Burgomaster et al., In the last decades the consumption of sugars in food and beverages has risen alarmingly and this is known to be associated with increased risk factors for CVD including dyslipidemia, hypertension, diabetes, or non‐alcoholic fatty liver diseases (Stanhope, The present study has some limitations that should be acknowledged. First, the study population comprised healthy overweight and obese adults that did not routinely participate in moderate‐ to high‐intensity aerobic exercise, and none had participated in resistance training in the last 3 month. As training status, sex and nutritional status of the individuals are determinants of metabolic response, our results may not be generalizable to other populations with different characteristics. Accordingly, these determining factors must be considered when interpreting results between studies. Second, the small sample size might be considered as a potential limitation, and future studies in larger cohorts including individuals with different characteristics (i.e., normal weight or physically active) are needed to further elucidate how acute SIT and metabolic responses are related. Third limitation is that we did not control the pre‐test nutritional habits of the participants, which could have affected metabolic responses. Future studies should examine whether diets high or low in carbohydrates or fats have a relevant effect on total oxidation rates of the substrates (Peric et al., The main strength of our study is that, to our knowledge, this is the first to investigate the effect of acute SIT on metabolic responses and substrate utilization after glucose consumption in inactive adults with overweight/obesity from the Latin‐American population. In addition, we provide measurements of these postprandial responses at multiple time points to better describe their temporal course.In conclusion, the present investigation indicates that acute SIT might have a positive effect on metabolic response to postprandial glucose and, therefore, it could be recommended for improving metabolism response in adults with overweight/obesity. The mechanism(s) involved in substrate utilization with SIT are not fully elucidated and the topic warrants further investigation.