Influence of vitamin D status on respiratory infection incidence and immune function during 4 months of winter training in endurance sport athletes.

The purpose of this study was to examine the influence of vitamin D status on mucosal and systemic immunity and the incidence, severity and duration of upper respiratory tract illness (URTI) episodes in endurance athletes during a 16-week winter training period. Blood was collected from 225 subjects at the start of the study and plasma was analysed for total 25-hydroxy vitamin D (25(OH)D) and cathelicidin concentration. Blood was also collected at the end of the study and analysed for 25(OH)D and antigen-stimulated cytokine production. Unstimulated saliva samples were obtained at the start and at 4-week intervals during the study period. Saliva samples were analysed for salivary antimicrobial peptides and proteins (AMPs). Weekly training and daily illness logs were kept. At the start and end of the study 38% and 55%, respectively, of the athlete cohort had inadequate (plasma 25(OH)D 30-50 nmol/L) or deficient (plasma 25(OH)D < 30 nmol/L) vitamin D status. There was a significantly higher proportion of subjects who presented with symptoms of URTI in the vitamin D deficient status group (initial plasma 25(OH)D < 30 nmol/L) during the study period than in the optimal vitamin D group (> 120 nmol/L) and the total number of URTI symptom days and the median symptom-severity score in the vitamin D deficient group was signifi- cantly higher than in the other groups. The plasma cathelicidin concentration positively correlated with the plasma 25(OH)D concentration and the saliva secretory immunoglobulin A (SIgA) secretion rate in the optimal vitamin D status group was significantly higher than in the other groups. Low vitamin D status was associated with lower pro-inflammatory cytokine production by monocytes and lymphocytes. Low vitamin D status could be an important determinant of URTI risk in endurance athletes and mucosal as well as systemic immunity may be modified via vitamin D-dependent mechanisms.