Maternal resistance exercise increases infant energy expenditure.

Maternal obesity decreases infant energy expenditure, subsequently predisposing infants to greater adiposity and weight gain. Conversely, some findings suggest that maternal exercise may increase infant energy expenditure; however, the impact of maternal exercise mode (i.e.

Exercise during pregnancy modulates infant cellular and whole-body adiposity.

Non-pharmaceutical interventions are needed to target the growing intergenerational cycle of obesity. We aimed to determine whether in utero exposure to different exercise doses during pregnancy directly reduces infant cellular and whole-body adiposity. Pregnant women completed ~24 weeks of supervised exercise training; for standardization of exercise analysis (frequency, intensity, time, and volume-FIT-V), metrics were assessed from 16 to 36 weeks.

Sex-Specific Skeletal Muscle Gene Expression Responses to Exercise Reveal Novel Direct Mediators of Insulin Sensitivity Change.

Background: Understanding the causal pathways, systems, and mechanisms through which exercise impacts human health is complex. This study explores molecular signaling related to whole-body insulin sensitivity (Si) by examining changes in skeletal muscle gene expression. The analysis considers differences by biological sex, exercise amount, and exercise intensity to identify potential molecular targets for developing pharmacologic agents that replicate the health benefits of exercise.

Effects of Weight Loss and Weight Maintenance on Lipoprotein Insulin Resistance Scores in Adults with Overweight and Obesity.

An elevated lipoprotein insulin resistance (LP-IR) score corresponds to insulin resistance in adults with overweight and obesity, yet data are lacking regarding the impact of exercise interventions on LP-IR. The purpose of this secondary analysis was to evaluate the effects of a weight loss and weight maintenance intervention on LP-IR score in adults with overweight and obesity. Thirty sedentary adults with overweight and obesity completed a 10-week OPTIFAST weight loss program with supervised aerobic exercise to achieve clinical weight loss (CWL) (≥7% from baseline).

Paternal obesity decreases infant MSC mitochondrial functional capacity.

Besides the well-recognized influence of maternal health on fetal in utero development, recent epidemiological studies appoint paternal preconception metabolic health as a significant factor in shaping fetal metabolic programming and subsequently offspring metabolic health; however, mechanisms behind these adaptations remain confined to animal models. To elucidate the effects of paternal obesity (P-OB) on infant metabolism in humans, we examined mesenchymal stem cells (MSCs), which give rise to infant tissue, remain involved in mature tissue maintenance, and resemble the phenotype of the offspring donor. Here, we assessed mitochondrial functional capacity, content, and insulin action in MSC from infants of fathers with overweight [body mass index (BMI: 25-30 kg/m); paternal overweight (P-OW)] or obesity (BMI ≥ 30 kg/m; P-OB) while controlling for maternal intrauterine environment.