Endurance training in early life results in long‐term programming of heart mass in rats. Issue 4 (February 2016)

• Record Type: Journal Article
• Authors: Wadley, Glenn D.; Laker, Rhianna C.; McConell, Glenn K.; Wlodek, Mary E.
• Is Part Of: Physiological reports. Volume 4:Issue 4(2016:Feb.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2016-02
• Subjects: Endurance training -- fetal programming -- heart hypertrophy; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12720
• Languages: English
• ISSNs: 2051-817X

Abstract

Abstract: Being born small for gestational age increases the risk of developing adult cardiovascular and metabolic diseases. This study aimed to examine if early‐life exercise could increase heart mass in the adult hearts from growth restricted rats. Bilateral uterine vessel ligation to induce uteroplacental insufficiency and fetal growth restriction in the offspring (Restricted) or sham surgery (Control) was performed on day 18 of gestation in WKY rats. A separate group of sham litters had litter size reduced to five pups at birth (Reduced litter), which restricted postnatal growth. Male offspring remained sedentary or underwent treadmill running from 5 to 9 weeks (early exercise) or 20 to 24 weeks of age (later exercise). Remarkably, in Control, Restricted, and Reduced litter groups, early exercise increased ( P < 0.05) absolute and relative (to body mass) heart mass in adulthood. This was despite the animals being sedentary for ~4 months after exercise. Later exercise also increased adult absolute and relative heart mass ( P < 0.05). Blood pressure was not significantly altered between groups or by early or later exercise. Phosphorylation of Akt Ser 473 in adulthood was increased in the early exercise groups but not the later exercise groups. Microarray gene analysis and validation by real‐time PCR did not reveal any long‐term effects of early exercise on the expression of any individual genes. In summary, early exercise programs the heart for increased mass into adulthood, perhaps by an upregulation of protein synthesis based on greater phosphorylation of Akt Ser 473 . Abstract : Being born small for gestational age increases the risk of developing adult cardiovascular and metabolic diseases. This study aimed to examine if early‐life exercise could increase heart mass in the adult hearts from growth restricted rats. In all groups, exercise early in life (5–9 weeks of age) increased heart mass in adulthood (24 weeks of age) despite the animals being sedentary for ~4 months. Greater cardiac phosphorylation of Akt Ser 473 in adulthood supports an upregulation of processes involved in cardiac growth due to exercise in early life. However, further work is required to establish the molecular mechanisms responsible for these novel findings.