The impact of ustekinumab and tumor necrosis factor antagonists on extraintestinal manifestations of Crohn's disease: a systematic review and meta-analysis.

Sedentary (SED) behavior has emerged as a significant modifiable risk factor contributing to increased morbidity and mortality []. Despite substantial evidence supporting the health benefits of physical activity, a large proportion of the US population remains in the low physical activity category, with this trend worsening across generations []. Pregnant individuals, in particular, spend about half of their day in SED behaviors, which have been linked to increased maternal complications, including adverse cardiometabolic changes, such as gestational diabetes, impaired glucose metabolism, and elevations in blood pressure, cholesterol, and triglyceride levels []. Importantly, these adverse cardiometabolic changes in pregnancy can negatively impact the maternal in utero environment, influencing fetal nutrition and outcomes [, , ]. SED behavior also contributes to weight gain, with over 60% of pregnant women in the United States classified as either overweight or obese [, ]. In both animal models and clinical populations, SED behavior as well as maternal obesity increases the risk for obesity, metabolic syndrome, and hypertension in offspring [, , ]. For example, infants born to overweight or obese mothers have decreased energy expenditure associated with higher body mass index and adiposity [, ]. This adverse metabolic phenotype has been linked to alterations in neural circuit development in animal models, with maternal obesity and overnutrition disrupting appetite‐regulating peptides in the hypothalamus []. Taken together, maternal SED behavior as well as maternal obesity can adversely impact metabolic, cardiovascular, and neurodevelopmental outcomes in offspring. Given these concerns, clinical research has begun to investigate preventative health interventions during pregnancy to mitigate the adverse effects of maternal SED behavior. In this regard, exercise during pregnancy can reduce maternal weight gain and adiposity, particularly in the latter half of gestation []. Additionally, exercise during pregnancy improves oral glucose tolerance and decreases the risk of gestational diabetes [, , ]. More recently, clinical studies have focused on the impact of exercise interventions during pregnancy on fetal outcomes. Moderate‐intensity exercise during pregnancy has been linked to improved maternal and fetal morbidity and mortality []. For example, maternal exercise has been shown to increase infant energy expenditure, result in lighter and leaner offspring [, ], as well as improve offspring cognitive development, including oral and motor skills []. Consistent with these clinical findings, maternal exercise has been reported to improve offspring metabolic health in rodent models, including improvements in glucose homeostasis and body composition [, , , ]. In these rodent models, the effects of maternal exercise on metabolic outcomes were largely studied in offspring later in life, between 6 months and 1 year of age. It remains unclear if similar changes occur earlier in life. In addition, the molecular mechanisms by which exercise during pregnancy benefits the metabolic health of offspring remain poorly understood. To address these gaps, in this exploratory study, we examined relationships between maternal exercise and offspring metabolic health at adolescent and early adulthood stages. Our findings suggest that maternal exercise is associated with alterations in adipose distribution and improved markers of adipose metabolic health in offspring, in the absence of changes in body mass and glucose homeostasis.