Influence of Maternal Exercise on Glucose and Lipid Metabolism in Offspring Stem Cells: ENHANCED by Mom
Related Experiment Video
Updated: Sep 24, 2025

Author Spotlight: Enhancing the Offspring Health in Rats with Maternal Exercise During Pregnancy
Published on: April 5, 2024
Alec Chaves1,2,3, Luke A Weyrauch1,2,3, Donghai Zheng1,2,3
1Department of Kinesiology, East Carolina University, Greenville, NC 27834, USA.
Context:
Recent preclinical data suggest exercise during pregnancy can improve the metabolic phenotype not only of the mother, but of the developing offspring as well. However, investigations in human offspring are lacking.
Objective:
To characterize the effect of maternal aerobic exercise on the metabolic phenotype of the offspring's mesenchymal stem cells (MSCs).
Design:
Randomized controlled trial.
Setting:
Clinical research facility.
Patients:
Healthy female adults between 18 and 35 years of age and ≤ 16 weeks' gestation.
Intervention:
Mothers were randomized into 1 of 2 groups: aerobic exercise (AE, n = 10) or nonexercise control (CTRL, n = 10). The AE group completed 150 minutes of weekly moderate-intensity exercise, according to American College of Sports Medicine guidelines, during pregnancy, whereas controls attended stretching sessions.
Main Outcome Measures:
Following delivery, MSCs were isolated from the umbilical cord of the offspring and metabolic tracer and immunoblotting experiments were completed in the undifferentiated (D0) or myogenically differentiated (D21) state.
Results:
AE-MSCs at D0 had an elevated fold-change over basal in insulin-stimulated glycogen synthesis and reduced nonoxidized glucose metabolite (NOGM) production (P ≤ 0.05). At D21, AE-MSCs had a significant elevation in glucose partitioning toward oxidation (oxidation/NOGM ratio) compared with CTRL (P ≤ 0.05). Immunoblot analysis revealed elevated complex I expression in the AE-MSCs at D21 (P ≤ 0.05). Basal and palmitate-stimulated lipid metabolism was similar between groups at D0 and D21.
Conclusions:
These data provide evidence of a programmed metabolic phenotype in human offspring with maternal AE during pregnancy.
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