CIRCULATING VITAMIN D IS UNAFFECTED DURING β-ADRENERGIC RECEPTOR STIMULATION, WITH OR WITHOUT CO-INFUSION OF VITAMIN C

Abstract

Vitamin D is essential for proper physiological function. Deficiency is clinicallydetermined by measuring circulating concentration; however, due to its lipophilic nature, most vitamin D is stored in adipose. Prevalence of vitamin D deficiency is high in adults with excessive adiposity (i.e., sedentary adults with body mass index (BMI)>25 kg/m2), suggesting deficiency may be more reflective of bioavailability than true deficiency. Acute exercise temporarily increases circulating concentrations of vitamin D, and this appears to coincide with increased release of free fatty acids from adipose tissue (i.e., lipolysis), a process mediated by beta-adrenergic receptor (βAR) stimulation. Our first aim is to determine if pharmaceutical βAR stimulation increases circulating vitamin D. In sedentary adults with BMI>25 kg/m2, oxidative stress attenuates βAR responsiveness. Our second aim is to determine if co-administration of the antioxidant, vitamin C, augments the vitamin D response to βAR stimulation. Using a randomized, placebo-controlled, crossover design, sedentary adults (5 male, 4 female, age 26±6 years, BMI 27.6±1.1 kg/m2 (mean±SD)) received three 30-minute continuous incremental intravenous doses of a non-selective βAR agonist (isoproterenol; 6, 12 and 24 ng/kg fat free mass/min) co-infused with either saline or vitamin C (0.05 g/kg fat free mass over 105 minutes). Blood was sampled and analyzed for vitamin D concentration at baseline and after each isoproterenol dose. During isoproterenol delivery, heart rate was progressively increased, indicative of successful βAR stimulation (52±11, 56±7, 66±7, and 81±19 bpm; p<0.001). Vitamin D concentration did not increase during βAR stimulation: plasma [25(OH)D3] (27.0±6.1, 27.4±7.0, 27.4±7.9, and 27.5±7.9 ng/mL, p=0.94); co-infusion of vitamin C did not influence the plasma [25(OH)D3] response (28.3±7.4, 28.1±7.6, 28.4±7.9 and 28.2±7.6 ng/mL, p=0.92). In contrast to our hypotheses, our preliminary data suggest that circulating vitamin D does not appear to be under βAR control, nor is it influenced by ascorbic acid-sensitive oxidative stress.