Abstract

Hypoadiponectinemia is associated with development of cardiovascular disease. We have previously reported that exercise-induced adaptations of the heart are impaired in mice with germline deletion of adiponectin. To determine a direct role for acute deletion of adiponectin in cardiac adaptations to exercise training, we exercise trained young adult mice with normal circulating adiponectin (wild type, WT) and mice in which adiponectin was acutely deleted (Cre-Lox conditional knockout system induced with Tamoxifen chow, AdipoKO) before undergoing 8 weeks of exercise training. Sedentary WT and AdipoKO mice were housed under similar cage conditions for 8 weeks. Lean mass and fat mass were assessed bi-weekly with Echo-MRI during the training and sedentary periods. Exercise tolerance, and cardiac function were assessed before and after completion of the 8 weeks training/sedentary period. Exercise training reduced fat mass and increased lean muscle mass in both WT mice and AdipoKO mice. Exercise training increased exercise tolerance in both WT mice and AdipoKO mice. Fractional shortening increased in WT mice, both sedentary and exercise trained, over the 8-week period, whereas fractional shortening tended to decrease in both sedentary and exercise trained AdipoKO mice. At the end of the 8-week exercise training/sedentary period, fractional shortening was significantly higher in WT mice compared to AdipoKO mice. At the end of the 8-week exercise training/sedentary period, ejection fraction was significantly higher in WT mice as compared to AdipoKO. Eight weeks of exercise training increased cardiac output in WT mice and cardiac output was higher in WT mice as compared to AdipoKO mice at the end of the 8-week exercise training/sedentary period. These data suggest that central cardiovascular adaptation is an important contributor to the increase in exercise tolerance that occurs in response to exercise training in WT mice. In contrast, in mice lacking adiponection, peripheral changes in metabolism and oxygen utilization are more likely contributors to the increase in exercise tolerance that occurs in response to exercise training. NIH R56AG068156 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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