Microvascular Function in Skeletal Muscle of Acute Adiponectin Knockout Mice

Adiponectin contributes to the regulation of vascular and metabolic functions in skeletal muscle. Although circulating adiponectin is known to increase with aerobic exercise training, a direct role for adiponectin in adaptation of microvasculature of skeletal muscle to aerobic exercise training has not been documented. 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. We determined skeletal muscle oxidative capacity, exercise tolerance, lean and fat mass, and we assessed reactivity of 1A arterioles from the gastrocnemius muscle. Exercise training increased exercise tolerance in both WT and AdipoKO mice. Exercise training increased lean mass and reduced fat mass in both WT and AdipoKO mice. Myogenic constriction to intraluminal pressure changes was increased by exercise training in gastrocnemius muscle 1A arterioles from both WT and AdipoKO mice. In contrast, phenylephrine-induced contractile responses were increased by exercise training in WT, but not AdipoKO mice. These data suggest that adiponectin is an important contributor to adaptations of contractile function that occur in skeletal muscle in response to exercise training; however, the training-induced increase in exercise tolerance and muscle mass that occurred in both WT and AdipoKO mice suggests that loss of adiponectin impacts smooth muscle function independently of metabolic adaptations in skeletal muscle. 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.