Maternal voluntary exercise protected female, but not male, offspring from HFHS-induced intrinsic myocardial dysfunction, preserving contractility and ventricular-arterial coupling.
Does maternal voluntary exercise prevent HFHS-induced intrinsic myocardial dysfunction in offspring?
Maternal voluntary exercise provides sex-specific protection against diet-induced myocardial dysfunction, preserving intrinsic cardiac mechanics in female but not male offspring.
Maternal metabolic health profoundly influences offspring cardiovascular risk, yet its interaction with lifelong obesogenic diet on intrinsic myocardial performance remains unclear. We hypothesized that maternal voluntary exercise modifies sex-specific myocardial adaptations to a high-fat, high-sucrose (HFHS) diet. HFHS-fed dams were assigned to sedentary or exercise groups. Offspring were weaned onto chow or HFHS diets, forming four groups: Sed-Chow, Ex-Chow, Sed-HFHS, and Ex-HFHS. At 29–32 weeks, cardiac function was assessed using pressure–volume loops and dobutamine challenge. Body and heart weights were recorded, and gene expression analysis targeted β-myosin heavy chain (Myh7), natriuretic peptide B (Nppb), SERCA2a (Atp2a2), phospholamban (Pln), and ECM-related genes. Ex-HFHS offspring exhibited the greatest body mass, particularly males. Heart weight-to-tibia length ratio was increased exclusively in Ex-HFHS offspring of both sexes, relative to all other groups. Sed-HFHS offspring showed reduced ejection fraction (%EF), while maternal exercise improved systolic function in both sexes. Striking sex differences emerged in load-independent indices: Ex-HFHS females demonstrated higher end-systolic elastance (Ees), lower end-diastolic elastance (Eed), and improved ventricular-arterial coupling ratio (Ees/Ea), indicating preserved contractility, diastolic stiffness, and ventricular–arterial coupling. Dobutamine challenge revealed superior contractile reserve in females, with greater increases in Ees, Ees/Ea, and reductions in end-systolic volume (ESV) and isovolumic relaxation constant (Tau). HFHS males lacked load-independent reserve; preload recruitable stroke work (PRSW) increased only in Sed-HFHS males. ECM-related genes (Col3a1, Col8a1, Timp1) were selectively elevated in male Ex-HFHS hearts. Maternal exercise confers robust protection against HFHS-induced intrinsic myocardial dysfunction in females, but not males, highlighting profound sex-specific differences in cardiac mechanics and stress adaptability. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Fang et al. (Fri,) conducted a other in HFHS-induced myocardial dysfunction. Maternal voluntary exercise vs. Sedentary maternal group was evaluated on Cardiac function assessed via pressure-volume loops and dobutamine challenge. Maternal voluntary exercise protected female, but not male, offspring from HFHS-induced intrinsic myocardial dysfunction, preserving contractility and ventricular-arterial coupling.