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Research Project: Impact of Maternal Influence and Early Dietary Factors on Child Growth, Development, and Metabolic Health

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Title: Early life exercise training counters metabolic perturbations imparted by low parental cardiorespiratory fitness

Author
item SADLER, DANIEL - University Arkansas For Medical Sciences (UAMS)
item TREAS, LILLIE - Arkansas Children'S Hospital
item ROSS, TAYLOR - Arkansas Children'S Hospital
item SIKES, JAMES - Arkansas Children'S Hospital
item BRITTON, STEVEN - University Of Michigan
item KOCH, LAUREN - University Of Toledo
item BORSHEIM, ELISABET - University Arkansas For Medical Sciences (UAMS)
item PORTER, CRAIG - University Arkansas For Medical Sciences (UAMS)

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/1/2023
Publication Date: N/A
Citation: N/A

Interpretive Summary: Inherited cardiorespiratory fitness (CRF) influences early life bioenergetics and metabolic health. We tested the hypothesis that early life exercise training would overcome whole-body and tissue metabolic defects imparted by low CRF. At 26 days of age, rat low-capacity runners (LCR, n=20) and high-capacity runners (HCR, n=20) generated by artificial selection were assigned to either sedentary control (CTRL, n=10) or voluntary wheel running (VWR, n=10) for 6 weeks. Our results reveal early life exercise training partially overcomes the metabolic phenotype imparted by low intrinsic CRF, although proteomic adaptations to early exercise training remain influenced by intrinsic CRF.

Technical Abstract: Introduction: Low cardiorespiratory fitness (CRF) is associated with a greater risk for metabolic disease. The potential for early life exercise training to overcome metabolic perturbations imparted by low intrinsic CRF remains unknown. We tested the hypothesis that early life exercise training would overcome whole-body and tissue metabolic defects imparted by low CRF. Methods: At 26 days of age, rat low-capacity runners (LCR, n=20) and high-capacity runners (HCR, n=20) generated by artificial selection were assigned to either sedentary control (CTRL, n=10) or voluntary wheel running (VWR, n=10) for 6 weeks. Post-intervention, whole-body metabolic phenotyping was performed, and the respiratory function of isolated skeletal muscle and liver mitochondria assayed. Quantitative proteomics were performed on tissue samples. Results and discussion: HCR-VWR performed 1.8-fold greater volume of wheel running than LCR-VWR (P<0.001). In LCR, VWR reduced body fat (P<0.001), increased total daily energy expenditure (+16%, P=0.030), and enhanced glucose tolerance (P=0.040). Muscle mitochondrial respiratory function was unaffected by VWR in both strains, although VWR increased muscle mitochondrial protein content (both P<0.05). VWR enhanced the respiratory capacity of HCR hepatic mitochondria (+23%, P=0.040). Proteomic analyses revealed lower capacity for fatty acid oxidation in muscle and liver of LCR-CTRL versus HCR-CTRL, which was not rescued by VWR. VWR reduced hepatic pyruvate kinase abundance in both strains (both P<0.013), indicating VWR may shift fuel preferences of hepatic mitochondria. These results reveal early life exercise training partially overcomes the metabolic phenotype imparted by low intrinsic CRF, although proteomic adaptations to early exercise training remain influenced by intrinsic CRF.