Previous Page
SPORTS MEDICINE VITAMIN D DEFICIENCY
BY DR BRUCE HAMILTON AND DR HAKIM CHALABI, SPORTS PHYSICIANS
INTRODUCTION What is vitamin D? Vitamin D is a steroid, derived from cholesterol in the skin under the influence of sunlight. Its active form is now known to act on most tissues and organs. Unfortunately it was named a vitamin in the early twentieth century, but in reality acts more like a hormone and has multiple systemic effects that we are only now beginning to understand fully. Vitamin D deficiency is endemic in many regions, with incidence increasing in many countries, and of course athletes have not been spared this trend. It seems that even skateboarders in Hawaii have been shown to be deficient in the vitamin.
Vitamin D and athletes The impact of vitamin D deficiency on the performance of athletes is not well described, but recent publications suggest that a deficiency can have a marked impact on physical performance. There are now several mechanisms that implicate vitamin D pathways in muscle structure and function, and there is some speculation about how it affects both muscle performance and injury profiles. Here we will briefly discuss the role of vitamin D in the body, and the mechanisms by which it may exert an effect on muscle structure and function.
Production of vitamin D Vitamin D is obtained in two main ways:
Vitamin D deficiency is common, even in groups previously not considered to be at risk. This article describes how vitamin D is utilised, its roles in the body and the mechanisms by which it may influence muscle structure and function, with reference to some recent research findings on functional ability and loss of muscle mass. There is guidance on recognising the signs of deficiency whether you are dealing with elite or recreational athletes or patients with atypical aches and pains. It also highlights the pitfalls of diagnosis and measurement, and will guide you through the current best management options.
n Via ultraviolet rays from the sun influencing the skin. n Through the diet from fortified cereals, oily fish and egg yolk and some yeast products. Ultraviolet B radiation (with a
wavelength of 290–315nm) acts on the skin to convert 7-dehydrocholesterol to pre-vitamin D3
of the skin, pre-vitamin D3
. In the dermis is
rapidly converted to vitamin D3 (cholecalciferol), before being converted
to 25-hydroxycholecalciferol-vitamin D (25(OH)D) in the liver. Vitamin D intoxication from sunlight exposure is prevented because sunlight destroys excess pre-vitamin D3
(1).
A final hydroxylation of 25(OH)D into the active form of vitamin D – 1,25 hydroxyvitamin D (1,25(OH)2
D) or
calcitriol – occurs in the kidneys. This final step is tightly regulated by parathyroid hormone (PTH), serum calcium and phosphorus levels (Fig. 1). Note that the term “vitamin D” refers to the metabolites and other analogues of these substances.
LIVER
1-alpha hydroxylase
parathyroid hormone
phosphorus calcium
vitamin D3
25-hydroxyvitamin D (25(OH)2D)
KIDNEYS
25-hydroxyvitamin D 1a-hydroxylase
1,25-dihydroxyvitamin D (1,25(OH)2D)
release of 1,25(OH)2D 11 circulation
Figure 1: Main steps in the production of vitamin D in the skin, liver and kidneys
7–dehydrocholesterol (DHC)
SKIN
SUNLIGHT ultraviolet B rays
Pre-vitamin D3 HEAT (cholecalciferol) vitamin D3 circulation