Vitamin D status modulates innate immune responses and metabolomic profiles following acute prolonged cycling

The influence of vitamin D status on exercise-induced immune dysfunction remains unclear. The aim of this study was to investigate the effects of vitamin D status (circulating 25(OH)D) on innate immune responses and metabolomic profiles to prolonged exercise.

Twenty three healthy, recreationally active males (age 25 ± 7 years; maximal oxygen uptake [[Formula: see text]max] 56 ± 9 mL·kg^-1·min^-1), classified as being deficient (n = 7) or non-deficient n = 16) according to plasma concentrations of 25(OH)D, completed 2.5 h of cycling at 15% Δ (~ 55-60% [Formula: see text]max). Venous blood and unstimulated saliva samples were obtained before and after exercise.

Participants with deficient plasma 25(OH)D on average had lower total lymphocyte count (mean difference [95% confidence interval], 0.5 cells × 10⁹ L [0.1, 0.9]), p = 0.013) and greater neutrophil:lymphocyte ratio (1.3 cells × 10⁹ L, [0.1, 2.5], p = 0.033). The deficient group experienced reductions from pre-exercise to 1 h post-exercise (- 43% [- 70, - 15], p = 0.003) in bacterial stimulated elastase in blood neutrophils compared to non-deficient participants (1% [- 20, 21], p = 1.000) Multivariate analyses of plasma metabolomic profiles showed a clear separation of participants according to vitamin D status. Prominent sources of variation between groups were purine/pyrimidine catabolites, inflammatory markers (linoleic acid pathway), lactate and tyrosine/adrenaline.

These findings provide evidence of the influence of vitamin D status on exercise-induced changes in parameters of innate immune defence and metabolomic signatures such as markers of inflammation and metabolic stress.