BSPED2012 Oral Communications Oral Communications 2 (10 abstracts)
Newcastle University, Newcastle Upon Tyne, UK.
Introduction: Mitochondria are critical organelles which generate most of the energy (ATP) in the eukaryotic cell by oxidative phosphorylation. Impaired mitochondrial function will, therefore, restrict myocellular function. Vitamin D deficiency is widely prevalent with fatigue amongst its commonest manifestation. 31P-MRS is a non-invasive technique used to measure skeletal muscle bioenergetics in vivo. We have examined the relationship between vitamin D and mitochondrial oxidative capacity.
Methods: We evaluated skeletal muscle bioenergetics using 31P-MRS in 64 volunteers. Resting metabolites and parameters of oxidative phosphorylation and peripheral vascular supply τ1/2 PCr and proton efflux were calculated using a validated exercise protocol. Regression analysis was undertaken to determine the predictors of oxidative phosphorylation (Minitab v16). Serum 25OHD was used as a surrogate of vitamin D status. Body fat assessment was undertaken using bio-impedance.
Results: Only serum 25OHD was a significant predictor of τ1/2PCr (P=0.012) in multiple regression analysis. In order to describe the relationship between serum 25OHD and τ1/2 PCr, a fitted line model was created. A negative correlation between serum 25OHD and τ1/2 PCr (r=−0.42, P=0.009) suggests that mitochondrial oxidative phosphorylation potential decreases with diminishing serum 25OHD levels. Vitamin D was negatively correlated with body fat% (r=−0.36, P=0.019) but no relationship existed between τ1/2 PCr and body fat%. There was no relationship between serum 25OHD and proton efflux.
Conclusion: Serum 25OHD may facilitate mitochondrial oxidative phosphorylation. The coupling efficiency of oxidative phosphorylation is correlated with many factors including hormone-responsive elements on the mitochondrial genome and our data suggest that vitamin D may modulate mitochondrial energy transduction. This may represent the bioenergetic basis for the fatigue experienced by vitamin D deficient adolescents and adults, although further studies are required to establish causality.