https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Decreased ATP production and myocardial contractile reserve in metabolic heart disease https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33017 ~ATP), c) the rate of ATP production and d) flux through the creatine kinase (CK) reaction. At the lowest workload, the diastolic pressure-volume relationship was shifted upward in HFHS hearts, indicative of diastolic dysfunction, whereas systolic function was preserved. At this workload, the rate of ATP synthesis was decreased in HFHS hearts, and was associated with decreases in both [PCr] and ΔG~ATP. Higher work demands unmasked the inability of HFHS hearts to increase systolic function and led to a further decrease in ΔG~ATP to a level that is not sufficient to maintain normal function of sarcoplasmic Ca²⁺-ATPase (SERCA). While [ATP] was preserved at all work demands in HFHS hearts, the progressive increase in [ADP] led to a decrease in ΔG~ATP with increased work demands. Surprisingly, CK flux, CK activity and total creatine were normal in HFHS hearts. These findings differ from dilated cardiomyopathy, in which the energetic deficiency is associated with decreases in CK flux, CK activity and total creatine. Thus, in HFHS-fed mice with MHD there is a distinct metabolic phenotype of the heart characterized by a decrease in ATP production that leads to a functionally-important energetic deficiency and an elevation of [ADP], with preservation of CK flux.]]> Wed 24 Nov 2021 15:52:41 AEDT ]]> Energetic dysfunction is mediated by mitochondrial reactive oxygen species and precedes structural remodeling in metabolic heart disease https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48338 per se, is sufficient to cause contractile dysfunction in MHD.]]> Tue 14 Mar 2023 17:22:37 AEDT ]]>