Key result
Aerobic exercise reduces EF ~9% in adiponectin knockout mice, showing adiponectin is required for cardiac adaptations.
Why the study?
Does aerobic exercise training improve cardiac and coronary microvascular function in mice lacking adiponectin?
Does aerobic exercise training improve cardiac and coronary microvascular function in mice lacking adiponectin?
Adiponectin appears necessary for the beneficial cardiac and coronary microvascular adaptations typically induced by aerobic exercise training.
Adiponectin may mediate exercise cardiac benefits in mice; leaves open translation to human therapy or practice change.
We report that compensatory mechanisms contribute to the maintenance of cardiac and coronary microvascular function in sedentary mice in which adiponectin has been deleted; however, when mice lacking adiponectin are subjected to the physiological stress of exercise training, beneficial coronary microvascular and cardiac adaptations are compromised or absent.
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Caldwell et al. (2021) studied Adiponectin deficiency (n=73). Aerobic exercise training vs. Sedentary cage confinement was evaluated on Ejection fraction (p=<0.05). Aerobic exercise training reduced ejection fraction by 9% and fractional shortening by 12% in adiponectin knockout mice, demonstrating that adiponectin is required for beneficial cardiac adaptations to exercise.
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