We tested the hypothesis that adiponectin deficiency attenuates coronary microvascular and cardiac function and prevents exercise training-induced adaptations of the coronary microvasculature and the myocardium in adult mice. Adult wild-type (WT) or adiponectin knockout (adiponectin KO) mice underwent treadmill exercise training or remained sedentary for 8-10 weeks. Systolic and diastolic function were assessed before and after exercise training or cage confinement. Vasoreactivity of coronary resistance arteries was assessed at the end of exercise training or cage confinement. Before exercise training, ejection fraction and fractional shortening were similar in adiponectin KO and WT mice, but isovolumic contraction time was significantly lengthened in adiponectin KO mice. Exercise training increased ejection fraction (12%) and fractional shortening (20%) with no change in isovolumic contraction time in WT mice. In adiponectin KO mice, both ejection fraction (-9%) and fractional shortening (-12%) were reduced after exercise training, and these decreases were coupled to a further increase in isovolumic contraction time (20%). In sedentary mice, endothelium-dependent dilation to flow was higher in arterioles from adiponectin KO mice as compared to WT mice. Exercise training enhanced dilation to flow in WT mice, but decreased flow-induced dilation in adiponectin KO mice. These data suggest that compensatory mechanisms contribute to the maintenance of microvascular and cardiac function in sedentary mice lacking adiponectin; however, in the absence of adiponectin, coronary microvascular and cardiac adaptations to exercise training are compromised.
Isovolumic contraction time of right ventricle in d-transposition of great arteries.
